What are the signs of coma. How many types of coma exist. What causes coma. How can coma be prevented. What treatment options are available for coma patients.

Understanding Coma and Its Manifestations

A coma is a state of prolonged unconsciousness where an individual is unresponsive to external stimuli. It’s a serious medical condition that requires immediate attention and careful management. One of the most intriguing aspects of coma is the presence of involuntary movements, which can provide valuable insights into the patient’s condition and prognosis.

What are involuntary movements in coma patients?

Involuntary movements in coma patients are uncontrolled physical actions that occur without conscious effort. These can range from subtle twitches to more pronounced movements of the limbs or facial muscles. Understanding these movements is crucial for healthcare professionals as they can indicate various underlying conditions or complications.

Types of Coma and Associated Movements

Comas can be classified into several types based on their cause and severity. Each type may present with different patterns of involuntary movements.

• Traumatic coma: Caused by severe head injuries
• Toxic-metabolic coma: Results from poisoning or metabolic imbalances
• Anoxic coma: Occurs due to lack of oxygen to the brain
• Infectious coma: Caused by severe infections affecting the brain

How do involuntary movements differ among coma types?

The nature and pattern of involuntary movements can vary significantly depending on the type of coma. For instance, patients in a toxic-metabolic coma might exhibit tremors or myoclonus (sudden, brief muscle jerks), while those in an anoxic coma may display decerebrate or decorticate posturing, characterized by rigid extension or flexion of the limbs.

Diagnostic Approach to Abnormal Movements in Comatose Patients

Accurately diagnosing the cause of involuntary movements in coma patients is crucial for appropriate treatment and management. Healthcare professionals employ a systematic approach to evaluate these movements and their underlying causes.

What diagnostic tools are used to assess coma patients?

Several diagnostic tools and techniques are utilized to evaluate coma patients and their involuntary movements:

1. Neurological examination: Assessing pupil reactivity, reflexes, and response to stimuli
2. Electroencephalogram (EEG): Monitoring brain electrical activity
3. Neuroimaging: CT scans and MRI to visualize brain structure and detect abnormalities
4. Blood tests: Checking for metabolic imbalances, toxins, or infections
5. Continuous video EEG monitoring: To capture and analyze movement patterns

Common Causes of Involuntary Movements in Coma

Involuntary movements in coma patients can stem from various underlying conditions. Identifying these causes is essential for targeted treatment and improved patient outcomes.

What are the primary causes of involuntary movements in comatose patients?

Several factors can contribute to involuntary movements in coma patients:

• Seizures and status epilepticus
• Metabolic disturbances (e.g., hypoglycemia, electrolyte imbalances)
• Drug toxicity or withdrawal
• Brainstem or spinal cord injuries
• Neurodegenerative disorders
• Post-anoxic myoclonus

It’s important to note that sometimes, these movements may be misinterpreted as seizures when they are actually non-epileptic in nature. This highlights the importance of accurate diagnosis for appropriate treatment.

Prevention Strategies for Coma and Associated Complications

While not all cases of coma can be prevented, there are measures that can reduce the risk of certain types of coma and associated complications.

How can the risk of coma be minimized?

Preventive strategies for coma include:

• Wearing protective gear during high-risk activities to prevent traumatic brain injuries
• Managing chronic health conditions such as diabetes and hypertension
• Avoiding substance abuse and following prescribed medication regimens
• Seeking immediate medical attention for severe infections or signs of stroke
• Ensuring proper oxygenation during medical procedures

Additionally, early recognition and treatment of conditions that can lead to coma, such as diabetic ketoacidosis or severe infections, can significantly reduce the risk of coma onset.

Treatment Approaches for Coma Patients

The treatment of coma patients is complex and multifaceted, often requiring a team of specialists to address various aspects of care.

What are the primary treatment strategies for coma patients?

Treatment approaches for coma patients typically include:

1. Addressing the underlying cause (e.g., treating infections, managing metabolic imbalances)
2. Providing supportive care (e.g., mechanical ventilation, nutrition support)
3. Preventing complications (e.g., pressure ulcers, deep vein thrombosis)
4. Managing symptoms and involuntary movements
5. Implementing neurorehabilitation strategies as appropriate

In cases where involuntary movements are caused by seizures, anti-epileptic medications may be administered. For movements related to metabolic disturbances, correcting the underlying imbalance is crucial.

The Role of Neuroplasticity in Coma Recovery

Recent research has shed light on the importance of neuroplasticity in coma recovery. This refers to the brain’s ability to reorganize itself by forming new neural connections, which can be crucial in the healing process after brain injury.

How does neuroplasticity contribute to coma recovery?

Neuroplasticity plays a significant role in coma recovery through several mechanisms:

• Rewiring of neural pathways to compensate for damaged areas
• Strengthening of existing connections to improve function
• Formation of new synapses to facilitate information transfer
• Adaptation of brain regions to take on new roles

Harnessing the power of neuroplasticity through targeted interventions and stimulation techniques can potentially enhance recovery outcomes for coma patients.

Emerging Technologies in Coma Diagnosis and Treatment

Advancements in medical technology are continually improving our ability to diagnose, monitor, and treat coma patients. These innovations offer new hope for improved outcomes and deeper understanding of coma states.

What cutting-edge technologies are being used in coma care?

Several emerging technologies are making significant impacts in coma care:

1. Functional MRI (fMRI): Detecting brain activity in seemingly unresponsive patients
2. Transcranial magnetic stimulation (TMS): Potentially stimulating brain activity
3. Brain-computer interfaces: Allowing limited communication with some coma patients
4. Advanced EEG analysis techniques: Providing more detailed insights into brain function
5. Artificial intelligence algorithms: Assisting in prognosis prediction and treatment planning

These technologies not only aid in diagnosis and treatment but also offer valuable insights into the nature of consciousness and brain function in coma states.

Long-term Prognosis and Quality of Life After Coma

The long-term outlook for coma patients can vary widely depending on the cause, duration, and severity of the coma. Understanding potential outcomes is crucial for patients, families, and healthcare providers in making informed decisions about care and planning for the future.

What factors influence the long-term prognosis of coma patients?

Several key factors can impact the long-term prognosis of individuals who have experienced a coma:

• Cause of the coma (traumatic vs. non-traumatic)
• Duration of unconsciousness
• Age and overall health of the patient
• Presence and severity of secondary complications
• Timing and quality of initial treatment
• Access to comprehensive rehabilitation services

It’s important to note that recovery from coma is often a gradual process, and improvements can continue for months or even years after the initial injury. While some patients may make a full recovery, others may experience lasting physical, cognitive, or emotional challenges.

How can quality of life be optimized for coma survivors?

Optimizing quality of life for coma survivors involves a multifaceted approach:

1. Comprehensive rehabilitation programs tailored to individual needs
2. Ongoing medical management of any residual symptoms or complications
3. Psychological support for both patients and families
4. Assistive technologies to aid in daily activities and communication
5. Community reintegration programs and vocational support
6. Regular follow-up care to address evolving needs

By focusing on these aspects, healthcare providers and support systems can help coma survivors achieve the best possible quality of life, regardless of the extent of their recovery.

Ethical Considerations in Coma Care

The care of coma patients often involves complex ethical considerations, particularly when it comes to decision-making about ongoing treatment, life support, and end-of-life care. These issues require careful thought and often involve input from medical professionals, ethicists, patients’ families, and sometimes legal experts.

What are the key ethical issues in coma care?

Several ethical dilemmas commonly arise in the care of coma patients:

• Determining when to continue or withdraw life-sustaining treatments
• Balancing the potential for recovery against quality of life considerations
• Respecting patient autonomy when the patient cannot communicate
• Allocating limited healthcare resources
• Addressing conflicts between medical recommendations and family wishes
• Ensuring equitable access to advanced coma care and technologies

Navigating these ethical challenges requires open communication, cultural sensitivity, and a thorough understanding of both medical and ethical principles. Many healthcare institutions have ethics committees to help address these complex issues and provide guidance to healthcare providers and families.

How can healthcare providers support families in decision-making?

Healthcare providers can support families of coma patients in several ways:

1. Providing clear, honest, and compassionate communication about the patient’s condition and prognosis
2. Offering access to support services, including social workers and chaplains
3. Encouraging families to express their values and preferences
4. Explaining treatment options and their potential outcomes in understandable terms
5. Respecting cultural and religious beliefs that may influence decision-making
6. Facilitating family meetings to discuss care plans and address concerns

By providing comprehensive support and guidance, healthcare providers can help families navigate the challenging decisions associated with coma care, ensuring that choices align with the patient’s best interests and values.

Abnormal movements in critical care patients with brain injury: a diagnostic approach

1. Wijdicks EF, Hijdra A, Young GB, Bassetti CL, Wiebe S, Quality Standards Subcommittee of the American Academy of Nuerology Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006;67:203–10. doi: 10.1212/01.wnl.0000227183.21314.cd. [PubMed] [CrossRef] [Google Scholar]

2. Venkatesan A, Frucht S. Movement disorders after resuscitation from cardiac arrest. Neurologic Clin. 2006;24:123–32. doi: 10.1016/j.ncl.2005.11.001. [PubMed] [CrossRef] [Google Scholar]

3. Mirski MA, Varelas PN. Seizures and status epilepticus in the critically ill. Crit Care Clin. 2008;24:115–47. doi: 10.1016/j.ccc.2007.11.005. [PubMed] [CrossRef] [Google Scholar]

4. Benbadis SR, Chen S, Melo M. What’s shaking in the ICU? The differential diagnosis of seizures in the intensive care setting. Epilepsia. 2010;51:2338–40. doi: 10.1111/j.1528-1167.2010.02683.x. [PubMed] [CrossRef] [Google Scholar]

5. Fahn SJJ, Hallet M, Jenner P. Priniciples and practive of movement disorders. Philadelphia: Churchill Livingstone; 2007. [Google Scholar]

6. Beghi E, Regio V, Papantonio A, Bentivoglio AR, Fasano A, Fogli D, et al. Reliability of clinical diagnosis of dystonia. Neuroepidemiology. 2014;43:213–9. doi: 10.1159/000367628. [PubMed] [CrossRef] [Google Scholar]

7. Logroscino G, Livrea P, Anaclerio D, Aniello MS, Benedetto G, Cazzato G, et al. Agreement among neurologists on the clinical diagnosis of dystonia at different body sites. J Neurol Neurosurg Psychiatry. 2003;74:348–50. doi: 10.1136/jnnp.74.3.348. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

8. Sierra-Hidalgo F, Romero JP, Bermejo-Pareja F, et al. Inter-rater agreement in the clinical diagnosis of essential tremor: data from the NEDICES-2 Pilot Study. Tremor Other Hyperkinet Mov (N Y) 2014;4:tre-04-187-4774-3. [PMC free article] [PubMed] [Google Scholar]

9. Bateman DE. Neurological assessment of coma. J Neurol Neurosurg Psychiatry. 2001;71(Suppl 1):i13–7. [PMC free article] [PubMed] [Google Scholar]

10. Bauer G, Trinka E. Nonconvulsive status epilepticus and coma. Epilepsia. 2010;51:177–90. doi: 10.1111/j.1528-1167.2009.02297.x. [PubMed] [CrossRef] [Google Scholar]

11. Alfonsi P. Postanaesthetic shivering. Epidemiology, pathophysiology and approaches to prevention and management. Minerva Anestesiol. 2003;69:438–42. [PubMed] [Google Scholar]

12. Walther S, Strik W. Motor symptoms and schizophrenia. Neuropsychobiology. 2012;66:77–92. doi: 10.1159/000339456. [PubMed] [CrossRef] [Google Scholar]

13. Caroff SN, Mann SC. Neuroleptic malignant syndrome. Med Clin N Am. 1993;77:185–202. [PubMed] [Google Scholar]

14. Alarcon F, Gimenez-Roldan S. Systemic diseases that cause movement disorders. Parkinsonism Relat Disord. 2005;11:1–18. doi: 10.1016/j.parkreldis.2004.10. 003. [PubMed] [CrossRef] [Google Scholar]

15. Alarcon F, Zijlmans JC, Duenas G, Cevallos N. Post-stroke movement disorders: report of 56 patients. J Neurol Neurosurg Psychiatry. 2004;75:1568–74. doi: 10.1136/jnnp.2003.011874. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

16. Bladin CF, Alexandrov AV, Bellavance A, Bornstein N, Chambers B, Coté R, et al. Seizures after stroke: a prospective multicenter study. Arch Neurol. 2000;57:1617–22. doi: 10.1001/archneur.57.11.1617. [PubMed] [CrossRef] [Google Scholar]

17. Varelas P. Seizures in critical care: a guide to diagnosis and therapeutics. 2. New York: Humana Press; 2010. [Google Scholar]

18. Pozos RS, Israel D, McCutcheon R, Wittmers LE, Jr, Sessler D. Human studies concerning thermal-induced shivering, postoperative “shivering,” and cold-induced vasodilation. Ann Emerg Med. 1987;16:1037–41. doi: 10.1016/S0196-0644(87)80756-4. [PubMed] [CrossRef] [Google Scholar]

19. Hirsch LJ, Pang T, Claassen J, Chang C, Khaled KA, Wittman J, Emerson RG. Focal motor seizures induced by alerting stimuli in critically ill patients. Epilepsia. 2008;49:968–73. doi: 10.1111/j.1528-1167.2007.01481.x. [PubMed] [CrossRef] [Google Scholar]

20. Stevens RD, Bhardwaj A. Approach to the comatose patient. Crit Care Med. 2006;34:31–41. doi: 10.1097/01.CCM.0000194534.42661.9F. [PubMed] [CrossRef] [Google Scholar]

21. Towne AR, Waterhouse EJ, Boggs JG, Garnett LK, Brown AJ, Smith JR, Jr, DeLorenzo RJ. Prevalence of nonconvulsive status epilepticus in comatose patients. Neurology. 2000;54:340–5. doi: 10.1212/WNL.54.2.340. [PubMed] [CrossRef] [Google Scholar]

22. Wijdicks EF, Varelas PN, Gronseth GS, Greer DM, American Academy of Neurology Evidence-based guideline update: determining brain death in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2010;74:1911–8. doi: 10.1212/WNL.0b013e3181e242a8. [PubMed] [CrossRef] [Google Scholar]

23. Saposnik G, Basile VS, Young GB. Movements in brain death: a systematic review. Can J Neurol Sci. 2009;36:154–60. doi: 10.1017/S031716710000651X. [PubMed] [CrossRef] [Google Scholar]

24. Jung KY, Han SG, Lee KH, Chung CS. Repetitive leg movements mimicking periodic leg movement during sleep in a brain-dead patient. Eur J Neurol. 2006;13:e3–4. doi: 10.1111/j.1468-1331.2006.01270.x. [PubMed] [CrossRef] [Google Scholar]

25. Ropper AH. Unusual spontaneous movements in brain-dead patients. Neurology. 1984;34:1089–92. doi: 10.1212/WNL.34.8.1089. [PubMed] [CrossRef] [Google Scholar]

26. Ziai WC, Kaplan PW. Seizures and status epilepticus in the intensive care unit. Semin Neurol. 2008;28:668–81. doi: 10.1055/s-0028-1105978. [PubMed] [CrossRef] [Google Scholar]

27. Claassen J, Taccone FS, Horn P, Holtkamp M, Stocchetti N, Oddo M, Neurointensive Care Section of the European Society of Intensive Care Medicine Recommendations on the use of EEG monitoring in critically ill patients: consensus statement from the neurointensive care section of the ESICM. Intensive Care Med. 2013;39:1337–51. doi: 10.1007/s00134-013-2938-4. [PubMed] [CrossRef] [Google Scholar]

28. Hirsch LJ, Claassen J, Mayer SA, Emerson RG. Stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs): a common EEG phenomenon in the critically ill. Epilepsia. 2004;45:109–23. doi: 10.1111/j.0013-9580.2004.38103.x. [PubMed] [CrossRef] [Google Scholar]

29. Frucht S, Fahn S. The clinical spectrum of posthypoxic myoclonus. Mov Disord. 2000;15(Suppl 1):2–7. doi: 10.1002/mds.870150702. [PubMed] [CrossRef] [Google Scholar]

30. Logan A, Sangkachand P, Funk M. Optimal management of shivering during therapeutic hypothermia after cardiac arrest. Crit Care Nurse. 2011;31:e18–30. doi: 10.4037/ccn2011618. [PubMed] [CrossRef] [Google Scholar]

31. Mani R, Schmitt SE, Mazer M, Putt ME, Gaieski DF. The frequency and timing of epileptiform activity on continuous electroencephalogram in comatose post-cardiac arrest syndrome patients treated with therapeutic hypothermia. Resuscitation. 2012;83:840–7. doi: 10.1016/j.resuscitation.2012.02.015. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

32. Wijdicks EF, Parisi JE, Sharbrough FW. Prognostic value of myoclonus status in comatose survivors of cardiac arrest. Ann Neurol. 1994;35:239–43. doi: 10.1002/ana.410350219. [PubMed] [CrossRef] [Google Scholar]

33. Hui AC, Cheng C, Lam A, Mok V, Joynt GM. Prognosis following postanoxic myoclonus status epilepticus. Eur Neurol. 2005;54:10–3. doi: 10.1159/000086755. [PubMed] [CrossRef] [Google Scholar]

34. Young GB, Gilbert JJ, Zochodne DW. The significance of myoclonic status epilepticus in postanoxic coma. Neurology. 1990;40:1843–8. doi: 10.1212/WNL.40.12.1843. [PubMed] [CrossRef] [Google Scholar]

35. Khot S, Tirschwell DL. Long-term neurological complications after hypoxic-ischemic encephalopathy. Semin Neurol. 2006;26:422–31. doi: 10.1055/s-2006-948323. [PubMed] [CrossRef] [Google Scholar]

36. Bhatt MH, Obeso JA, Marsden CD. Time course of postanoxic akinetic-rigid and dystonic syndromes. Neurology. 1993;43:314–7. doi: 10.1212/WNL.43.2.314. [PubMed] [CrossRef] [Google Scholar]

37. Virmani T, Greene PE, Pearson TS. Delayed onset of progressive chorea after acute basal ganglia injury. Mov Disord. 2013;28:585–7. doi: 10.1002/mds.25436. [PubMed] [CrossRef] [Google Scholar]

38. Krauss JK, Pohle T, Borremans JJ. Hemichorea and hemiballism associated with contralateral hemiparesis and ipsilateral basal ganglia lesions. Mov Disord. 1999;14:497–501. doi: 10.1002/1531-8257(199905)14:3<497::AID-MDS1019>3.0.CO;2-X. [PubMed] [CrossRef] [Google Scholar]

39. Ropper AH. Hyperosmolar therapy for raised intracranial pressure. N Engl J Med. 2012;367:746–52. doi: 10.1056/NEJMct1206321. [PubMed] [CrossRef] [Google Scholar]

40. Diringer MN, Bleck TP, Claude Hemphill J, 3rd, Menon D, Shutter L, Vespa P, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care. 2011;15:211–40. doi: 10.1007/s12028-011-9605-9. [PubMed] [CrossRef] [Google Scholar]

41. Ghika-Schmid F, Ghika J, Regli F, Bogousslavsky J. Hyperkinetic movement disorders during and after acute stroke: the Lausanne Stroke Registry. J Neurol Sci. 1997;146:109–16. doi: 10.1016/S0022-510X(96)00290-0. [PubMed] [CrossRef] [Google Scholar]

42. Bansil S, Prakash N, Kaye J, Wrigley S, Manata C, Stevens-Haas C, Kurlan R. Movement disorders after stroke in adults: a review. Tremor Other Hyperkinet Mov (N Y) 2012;2:tre-02-42-195-1. [PMC free article] [PubMed] [Google Scholar]

43. Mehanna R, Jankovic J. Movement disorders in cerebrovascular disease. Lancet Neurol. 2013;12:597–608. doi: 10.1016/S1474-4422(13)70057-7. [PubMed] [CrossRef] [Google Scholar]

44. Devinsky O, Kelley K, Porter RJ, Theodore WH. Clinical and electroencephalographic features of simple partial seizures. Neurology. 1988;38:1347–52. doi: 10.1212/WNL.38.9.1347. [PubMed] [CrossRef] [Google Scholar]

45. Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS. Bratton SL, Chestnut RM, et al. Guidelines for the management of severe traumatic brain injury. XIII. Antiseizure prophylaxis. J Neurotrauma. 2007;24 Suppl 1:S83–6. [PubMed] [Google Scholar]

46. Lump D, Moyer M. Paroxysmal sympathetic hyperactivity after severe brain injury. Curr Neurol Neurosci Rep. 2014;14:494. doi: 10.1007/s11910-014-0494-0. [PubMed] [CrossRef] [Google Scholar]

47. O’Suilleabhain P, Dewey RB., Jr Movement disorders after head injury: diagnosis and management. J Head Trauma Rehabil. 2004;19:305–13. doi: 10.1097/00001199-200407000-00005. [PubMed] [CrossRef] [Google Scholar]

48. Krauss JK, Jankovic J. Head injury and posttraumatic movement disorders. Neurosurgery. 2002;50:927–39. [PubMed] [Google Scholar]

49. Wang DW, Yin YM, Yao YM. Advances in the management of acute liver failure. World J Gastroenterol. 2013;19:7069–77. doi: 10.3748/wjg.v19.i41.7069. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

50. Barrett KM. Neurologic manifestations of acute and chronic renal disease. Continuum. 2011;17:45–55. [PubMed] [Google Scholar]

51. Harris MK, Elliott D, Schwendimann RN, Minagar A, Jaffe SL. Neurologic presentations of hepatic disease. Neurologic Clin. 2010;28:89–105. doi: 10.1016/j.ncl.2009.09.016. [PubMed] [CrossRef] [Google Scholar]

52. Hirsch KG, Josephson SA. An update on neurocritical care for the patient with kidney disease. Adv Chronic Kidney Dis. 2013;20:39–44. doi: 10.1053/j.ackd.2012.09.003. [PubMed] [CrossRef] [Google Scholar]

53. Barton B, Zauber SE, Goetz CG. Movement disorders caused by medical disease. Semin Neurol. 2009;29:97–110. doi: 10.1055/s-0029-1213731. [PubMed] [CrossRef] [Google Scholar]

54. Young RR, Shahani BT. Asterixis: one type of negative myoclonus. Adv Neurol. 1986;43:137–56. [PubMed] [Google Scholar]

55. Oh SH, Lee KY, Im JH, Lee MS. Chorea associated with non-ketotic hyperglycemia and hyperintensity basal ganglia lesion on T1-weighted brain MRI study: a meta-analysis of 53 cases including four present cases. J Neurol Sci. 2002;200:57–62. doi: 10.1016/S0022-510X(02)00133-8. [PubMed] [CrossRef] [Google Scholar]

56. Newman RP, Kinkel WR. Paroxysmal choreoathetosis due to hypoglycemia. Arch Neurol. 1984;41:341–2. doi: 10.1001/archneur.1984.04050150123033. [PubMed] [CrossRef] [Google Scholar]

57. Yen DJ, Shan DE, Lu SR. Hyperthyroidism presenting as recurrent short paroxysmal kinesigenic dyskinesia. Mov Disord. 1998;13:361–3. doi: 10.1002/mds.870130231. [PubMed] [CrossRef] [Google Scholar]

58. Isaacs JD, Rakshi J, Baker R, Brooks DJ, Warrens AN. Chorea associated with thyroxine replacement therapy. Mov Disord. 2005;20:1656–7. doi: 10.1002/mds.20603. [PubMed] [CrossRef] [Google Scholar]

59. Kang EG, Jeon SJ, Choi SS, Song CJ, Yu IK. Diffusion MR imaging of hypoglycemic encephalopathy. Am J Neuroradiol. 2010;31:559–64. doi: 10.3174/ajnr.A1856. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

60. Tambyah PA, Ong BK, Lee KO. Reversible parkinsonism and asymptomatic hypocalcemia with basal ganglia calcification from hypoparathyroidism 26 years after thyroid surgery. Am J Med. 1993;94:444–5. doi: 10.1016/0002-9343(93)90159-M. [PubMed] [CrossRef] [Google Scholar]

61. Strawn JR, Keck PE, Jr, Caroff SN. Neuroleptic malignant syndrome. Am J Psychiatry. 2007;164:870–6. doi: 10.1176/ajp.2007.164.6.870. [PubMed] [CrossRef] [Google Scholar]

62. Velamoor VR, Norman RM, Caroff SN, Mann SC, Sullivan KA, Antelo RE. Progression of symptoms in neuroleptic malignant syndrome. J Nervous Mental Dis. 1994;182:168–73. doi: 10.1097/00005053-199403000-00007. [PubMed] [CrossRef] [Google Scholar]

63. Iqbal MM, Basil MJ, Kaplan J, Iqbal MT. Overview of serotonin syndrome. Ann Clin Psychiatry. 2012;24:310–8. [PubMed] [Google Scholar]

64. Haddad PM, Das A, Ashfaq M, Wieck A. A review of valproate in psychiatric practice. Expert Opin Drug Metab Toxicol. 2009;5:539–51. doi: 10.1517/17425250902911455. [PubMed] [CrossRef] [Google Scholar]

65. Friedman LS, Weinrauch LA, D’Elia JA. Metoclopramide-induced neuroleptic malignant syndrome. Arch Internal Med. 1987;147:1495–7. doi: 10.1001/archinte.1987.00370080133023. [PubMed] [CrossRef] [Google Scholar]

66. Dressler D, Benecke R. Diagnosis and management of acute movement disorders. J Neurol. 2005;252:1299–306. doi: 10.1007/s00415-005-0006-x. [PubMed] [CrossRef] [Google Scholar]

67. Pisani F, Oteri G, Costa C, Di Raimondo G, Di Perri R. Effects of psychotropic drugs on seizure threshold. Drug Saf. 2002;25:91–110. doi: 10.2165/00002018-200225020-00004. [PubMed] [CrossRef] [Google Scholar]

68. Morgan JC, Sethi KD. Drug-induced tremors. Lancet Neurol. 2005;4:866–76. doi: 10.1016/S1474-4422(05)70250-7. [PubMed] [CrossRef] [Google Scholar]

69. Murphy K, Delanty N. Drug-induced seizures. CNS Drugs. 2000;14:135–46. doi: 10.2165/00023210-200014020-00004. [CrossRef] [Google Scholar]

70. Bhidayasiri R, Truong DD. Chorea and related disorders. Postgrad Med J. 2004;80:527–34. doi: 10.1136/pgmj.2004.019356. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

71. Baizabal-Carvallo JF, Jankovic J. Movement disorders in autoimmune diseases. Mov Disord. 2012;27:935–46. doi: 10.1002/mds.25011. [PubMed] [CrossRef] [Google Scholar]

72. Pfister HW, Feiden W, Einhaupl KM. Spectrum of complications during bacterial meningitis in adults. Results of a prospective clinical study. Arch Neurol. 1993;50:575–81. doi: 10.1001/archneur.1993.00540060015010. [PubMed] [CrossRef] [Google Scholar]

73. Murthy S, Keystone J, Kissoon N. Infections of the developing world. Crit Care Clin. 2013;29:485–507. doi: 10.1016/j.ccc.2013.03.005. [PubMed] [CrossRef] [Google Scholar]

74. Sarrazin JL, Bonneville F, Martin-Blondel G. Brain infections. Diagn Interv Imaging. 2012;93:473–90. doi: 10. 1016/j.diii.2012.04.020. [PubMed] [CrossRef] [Google Scholar]

75. Michael BD, Solomon T. Seizures and encephalitis: clinical features, management, and potential pathophysiologic mechanisms. Epilepsia. 2012;53(Suppl 4):63–71. doi: 10.1111/j.1528-1167.2012.03615.x. [PubMed] [CrossRef] [Google Scholar]

76. Sejvar JJ, Marfin AA. Manifestations of West Nile neuroinvasive disease. Rev Med Virol. 2006;16:209–24. doi: 10.1002/rmv.501. [PubMed] [CrossRef] [Google Scholar]

77. Alarcon F, Maldonado JC, Rivera JW. Movement disorders identified in patients with intracranial tuberculomas. Neurologia. 2011;26:343–50. doi: 10.1016/j.nrl.2010.12.011. [PubMed] [CrossRef] [Google Scholar]

78. Alarcon F, Duenas G, Cevallos N, Lees AJ. Movement disorders in 30 patients with tuberculous meningitis. Mov Disord. 2000;15:561–9. doi: 10.1002/1531-8257(200005)15:3<561::AID-MDS1021>3.0.CO;2-K. [PubMed] [CrossRef] [Google Scholar]

79. Tschampa HJ, Herms JW, Schulz-Schaeffer WJ, Maruschak B, Windl O, Jastrow U, et al. Clinical findings in sporadic Creutzfeldt-Jakob disease correlate with thalamic pathology. Brain. 2002;125:2558–66. doi: 10.1093/brain/awf253. [PubMed] [CrossRef] [Google Scholar]

80. Garg RK, Karak B, Misra S. Neurological manifestations of malaria: an update. Neurol India. 1999;47:85–91. [PubMed] [Google Scholar]

81. Nash TE, Mahanty S, Loeb JA, Theodore WH, Friedman A, Sander JW, et al. Neurocysticercosis: a natural human model of epileptogenesis. Epilepsia. 2015;56:177–83. doi: 10.1111/epi.12849. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

82. Baizabal-Carvallo JF, Bonnet C, Jankovic J. Movement disorders in systemic lupus erythematosus and the antiphospholipid syndrome. J Neural Transm (Vienna) 2013;120:1579–89. doi: 10.1007/s00702-013-1023-z. [PubMed] [CrossRef] [Google Scholar]

83. Baizabal-Carvallo JF, Stocco A, Muscal E, Jankovic J. The spectrum of movement disorders in children with anti-NMDA receptor encephalitis. Mov Disord. 2013;28:543–7. doi: 10.1002/mds.25354. [PubMed] [CrossRef] [Google Scholar]

84. Hannawi Y, Hannawi B, Rao CP, Suarez JI, Bershad EM. Stroke-associated pneumonia: major advances and obstacles. Cerebrovasc Dis. 2013;35:430–43. doi: 10.1159/000350199. [PubMed] [CrossRef] [Google Scholar]

85. Chamorro A, Meisel A, Planas AM, Urra X, van de Beek D, Veltkamp R. The immunology of acute stroke. Nat Rev Neurol. 2012;8:401–10. doi: 10.1038/nrneurol.2012.98. [PubMed] [CrossRef] [Google Scholar]

86. Davis R, Dalmau J. Autoimmunity, seizures, and status epilepticus. Epilepsia. 2013;54(Suppl 6):46–9. doi: 10.1111/epi.12276. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

87. Rosenfeld MR, Titulaer MJ, Dalmau J. Paraneoplastic syndromes and autoimmune encephalitis: five new things. Neurol Clin Practice. 2012;2:215–23. doi: 10.1212/CPJ.0b013e31826af23e. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

88. Rosenfeld MR, Dalmau J. Paraneoplastic neurologic disorders: a brief overview. Memo. 2012;5:197–200. doi: 10.1007/s12254-012-0034-z. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

89. Hannawi Y, Goldsmith CE, Kass JS, Olar A, Ubogu EE, Kalkonde YV. A case of severe chronic progressive axonal polyradiculoneuropathy temporally associated with anti-CV2/CRMP5 antibodies. J Clin Neuromusc Dis. 2013;15:13–8. doi: 10.1097/CND.0b013e3182a04538. [PubMed] [CrossRef] [Google Scholar]

90. Serratrice G, Serratrice J. Continuous muscle activity, Morvan’s syndrome and limbic encephalitis: ionic or non ionic disorders? Acta Myol. 2011;30:32–3. [PMC free article] [PubMed] [Google Scholar]

91. Mocellin R, Walterfang M, Velakoulis D. Hashimoto’s encephalopathy: epidemiology, pathogenesis and management. CNS Drugs. 2007;21:799–811. doi: 10.2165/00023210-200721100-00002. [PubMed] [CrossRef] [Google Scholar]

92. Batchelor T, DeAngelis LM. Medical management of cerebral metastases. Neurosurg Clin N Am. 1996;7:435–46. [PubMed] [Google Scholar]

93. Lacy J, Saadati H, Yu JB. Complications of brain tumors and their treatment. Hematol Oncol Clin N Am. 2012;26:779–96. doi: 10.1016/j.hoc.2012.04.007. [PubMed] [CrossRef] [Google Scholar]

94. Thomas JE, Reagan TJ, Klass DW. Epilepsia partialis continua. A review of 32 cases. Arch Neurol. 1977;34:266–75. doi: 10.1001/archneur.1977.00500170020003. [PubMed] [CrossRef] [Google Scholar]

95. Bhatoe HS. Movement disorders caused by brain tumours. Neurol India. 1999;47:40–2. [PubMed] [Google Scholar]

96. Jr B. Stupor and Coma. In: Bradley WG, Daroff RB, Fenichel GM, Jankovic J, editors. Neurology in clinical practice. Philadelphia: Elsevier; 2008. pp. 39–58. [Google Scholar]

97. Sutter R, Stevens RD, Kaplan PW. Continuous electroencephalographic monitoring in critically ill patients: indications, limitations, and strategies. Crit Care Med. 2013;41:1124–32. doi: 10.1097/CCM.0b013e318275882f. [PubMed] [CrossRef] [Google Scholar]

Vegetative State and Minimally Conscious State – Neurologic Disorders

By

Kenneth Maiese

, MD, Rutgers University

Reviewed/Revised May 2022 | Modified Sep 2022

View Patient Education

A vegetative state is absence of responsiveness and awareness due to overwhelming dysfunction of the cerebral hemispheres, with sufficient sparing of the diencephalon and brain stem to preserve autonomic and motor reflexes and sleep-wake cycles. Patients may have complex reflexes, including eye movements, yawning, and involuntary movements to noxious stimuli, but show no awareness of self or environment. A minimally conscious state, unlike a vegetative state, is characterized by some evidence of awareness of self and/or the environment, and patients tend to improve. Diagnosis is clinical. Treatment is mainly supportive. Prognosis for patients with persistent deficits is typically bleak.

The vegetative state is a chronic condition that preserves the ability to maintain blood pressure (BP), respiration, and cardiac function, but not cognitive function. Hypothalamic and medullary brain stem functions remain intact to support cardiorespiratory and autonomic functions and are sufficient for survival if medical and nursing care is adequate. The cortex is severely damaged (eliminating cognitive function), but the reticular activating system (RAS) remains functional (making wakefulness possible). Midbrain or pontine reflexes may or may not be present. Patients have no awareness of self and interact with the environment only via reflexes. Seizure activity may be present but not be clinically evident.

Traditionally, a vegetative state that lasts > 1 month is considered to be a persistent vegetative state. However, a diagnosis of persistent vegetative state does not imply permanent disability because in very rare cases (eg, after traumatic brain injury), patients can improve, reaching a minimally conscious state or a higher level of consciousness.

The most common causes of a vegetative state and minimally conscious state are

• Traumatic brain injury Traumatic Brain Injury (TBI) Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs brain function. Diagnosis is suspected clinically and confirmed by imaging (primarily… read more

• Diffuse cerebral hypoxia

However, any disorder that results in brain damage can cause a vegetative state. Typically, a vegetative state occurs because the function of the brain stem and diencephalon resumes after coma, but cortical function does not.

In the minimally conscious state, unlike the vegetative state, there is evidence that patients are aware of themselves and/or their environment. Patients also tend to improve (ie, gradually become more conscious), but improvement is limited. This state may be the first indication of brain damage or may follow a vegetative state as people recover some function. Patients can transition between the vegetative state and minimally conscious state, sometimes for years after the original brain damage.

Patients in a vegetative state show no evidence of awareness of self or environment and cannot interact with other people. Purposeful responses to external stimuli are absent, as are language comprehension and expression.

The following are present in patients in a vegetative state:

• Signs of an intact reticular formation (eg, eye opening) and an intact brain stem (eg, reactive pupils, oculocephalic reflex)

• Sleep-wake cycles, not necessarily reflecting a specific circadian rhythm nor associated with the environment

• More complex brain stem reflexes, including yawning, chewing, swallowing, and, uncommonly, guttural vocalizations

• Sometimes arousal and startle reflexes (eg, loud sounds or blinking with bright lights may elicit eye opening)

• Sometimes watering and tearing of the eyes

• Sometimes the appearance of a smile or frown

• Spontaneous roving eye movements—usually slow, of constant velocity, and without saccadic jerks

The spontaneous roving eye movements may be misinterpreted as volitional tracking and can be misinterpreted by family members as evidence of awareness.

Patients cannot react to visual threat and cannot follow commands. The limbs may move, but the only purposeful motor responses that occur are primitive (eg, grasping an object that contacts the hand). Pain usually elicits a motor response (typically decorticate or decerebrate posturing) but no purposeful avoidance. Patients have fecal and urinary incontinence. Cranial nerve and spinal reflexes are typically preserved.

Rarely, brain activity, detected by functional MRI or electroencephalography (EEG), indicates a response to questions and commands even though there is no behavioral response (covert consciousness). The extent of patients’ actual awareness is not yet known. In most patients who have such brain activity, the vegetative state resulted from traumatic brain injury, not hypoxic encephalopathy.

Fragments of meaningful interaction with the environment are preserved. Patients in a minimally conscious state may do the following:

• Establish eye contact

• Purposefully grasp at objects

• Respond to commands in a stereotypic manner

• Answer with the same word

A vegetative state is suggested by characteristic findings (eg, no purposeful activity or comprehension) plus signs of an intact reticular formation. Diagnosis is based on clinical criteria. However, neuroimaging is indicated to rule out treatable disorders.

The vegetative state must be distinguished from the minimally conscious state. Both states can be permanent or temporary, and the physical examination may not reliably distinguish one from the other. Sufficient observation is needed. If observation is too brief, evidence of awareness may be overlooked. Some patients with severe Parkinson disease are misdiagnosed as being in a vegetative state.

CT or MRI can differentiate an ischemic infarct, an intracerebral hemorrhage, and a mass lesion involving the cortex or the brain stem. Magnetic resonance angiography can be used to visualize the cerebral vasculature after exclusion of a cerebral hemorrhage. Diffusion-weighted MRI is becoming the preferred imaging modality for following ongoing ischemic changes in the brain.

Positron emission tomography (PET), functional MRI, and single-photon emission computed tomography (SPECT) can be used to assess cerebral function (rather than brain anatomy). If the diagnosis of persistent vegetative state is in doubt, PET, SPECT, or functional MRI should be done. In some cases, these tests can show whether parts of the brain, such as the cortex, are still functioning even if it is not evident during clinical examination.

EEG is useful in assessing cortical dysfunction and identifying occult seizure activity.

Prognosis varies somewhat by cause and duration of the vegetative state. Prognosis may be better if the cause is a reversible metabolic condition (eg, toxic encephalopathy) than if the cause is neuronal death due to extensive hypoxia and ischemia or another condition. Also, younger patients may recover more motor function than older patients but not more cognition, behavior, or speech.

Recovery from a vegetative state is unlikely after 1 month if brain damage is nontraumatic and after 12 months if brain damage is traumatic. Even if some recovery occurs after these intervals, most patients are severely disabled. Rarely, improvement occurs late; after 5 years, about 3% of patients recover the ability to communicate and comprehend, but even fewer can live independently; no patients regain normal function.

If a vegetative state persists, most patients die within 6 months of the original brain damage. The cause is usually pulmonary infection, urinary tract infection, or multiple organ failure, or death may be sudden and of unknown cause. For most of the rest, life expectancy is about 2 to 5 years; only about 25% of patients live > 5 years. A few patients live for decades.

Most patients tend to recover consciousness but to a limited extent depending on how long the minimally conscious state has lasted. The longer it has lasted, the less chance of patients recovering higher cortical function. Prognosis may be better if the cause is traumatic brain injury.

Rarely, patients regain clear but limited awareness after years of coma, called awakenings by the news media.

• Supportive care

Supportive care is the mainstay of treatment for patients in a vegetative state or minimally conscious state; it should include the following:

• Preventing systemic complications due to immobilization (eg, pneumonia, urinary tract infection, thromboembolic disease)

• Providing good nutrition

• Preventing pressure ulcers Prevention Pressure injuries are areas of necrosis and often ulceration (also called pressure ulcers) where soft tissues are compressed between bony prominences and external hard surfaces. They are caused… read more

• Providing physical therapy to prevent limb contractures

Vegetative state has no specific treatment. Decisions about life-sustaining care should involve social services, the hospital ethics committee, and family members. Maintaining patients, especially those without advanced directives Advance Directives Advance directives are legal documents that extend a person’s control over health care decisions in the event that the person becomes incapacitated. They are called advance directives because… read more to guide decisions about terminating treatment, in a prolonged vegetative state raises ethical and other (eg, resource utilization) questions.

Most patients in a minimally conscious state do not respond to specific treatments. However, in some cases, treatment with zolpidem, apomorphine, or amantadine can lead to improvement in neurologic responsiveness for as long as the drug is continued.

A growing number of studies are evaluating the effects of providing music interventions during disorders of consciousness (1 Treatment reference A vegetative state is absence of responsiveness and awareness due to overwhelming dysfunction of the cerebral hemispheres, with sufficient sparing of the diencephalon and brain stem to preserve. .. read more ). Some studies show that music therapy may lead to positive behavioral effects and return to normal physiologic responses. Results should be interpreted with caution because research in this area has thus far been limited.

• 1. Li X, Li C, Hu N, Wang T: Music interventions for disorders of consciousness: A systematic review and meta-analysis. J Neurosci Nurs 52 (4): 146–151, 2020. doi: 10.1097/JNN.0000000000000511

• Vegetative state is typically characterized by absence of responsiveness and awareness due to overwhelming dysfunction of the cerebral hemispheres, intact brain stem function, and sometimes the simulation of awareness despite its absence.

• Minimally conscious state differs from vegetative state in that patients have some interaction with the environment and tend to improve over time.

• Diagnosis requires exclusion of other disorders and often prolonged observation, particularly to differentiate vegetative state, minimally conscious state, and Parkinson disease.

• Prognosis tends to be poor, particularly for patients in a vegetative state.

• Treatment is mainly supportive.

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Coma state – Adamant Medical Clinic

Adamant
medical clinic

St. Petersburg, embankment of the river Moika, 78.

+7 (812) 740-20-90

Content:

Coma – a condition in which a person is unconscious and does not respond to any external stimuli, reflexes and vital functions of the body are disturbed. It is caused by mechanical damage to the brain – hemorrhages, traumas and tumors or infectious diseases. The doctor and technician of the Adamant Medical Clinic prolong the life of patients who are in an unconscious state, and also contribute to the complex recovery of the body after a coma state.

Coma symptoms depend on the severity of the condition:

1. Precoma:

   • confusion;
   • drowsiness and lethargy, sometimes reverse symptoms are observed due to excessive excitement;
   • reflexes are preserved.

2. Coma 1st degree

   • delayed reaction;
   • stun;
   • the patient is difficult to make contact;
   • reflexes can be either excessively increased or decreased.

3. Coma 2nd degree

   • deep dream;
   • rare involuntary movements of the limbs;
   • noisy and irregular breathing;
   • involuntary urination and defecation;
   • the patient does not make contact.

4. Coma 3rd degree

   • there is no consciousness;
   • there is no reaction to pain, light, and in general any external stimuli;
   • pupils are dilated;
   • body temperature and blood pressure decrease;
   • consciousness is disturbed.

5. Coma 4th degree

   • deep disturbance of consciousness;
   • the absence of all reflexes;
   • body temperature and blood pressure decrease;
   • muscles completely lose their tone;
   • independent breathing of the patient is difficult, it is necessary to connect to the device.

Coma is a serious condition that can develop rapidly, or within a few hours or even days. Remember that at the first sign of it, you need to see a doctor! Calling an ambulance at the Adamant Medical Clinic in time will help you avoid serious consequences and guarantee you qualified assistance. Otherwise, death is possible.

Coma. What you need to know – TASS

How to distinguish someone from fainting? How long does it last and what are the chances of a full recovery? Is artificial coma also dangerous? The main thing about the mysterious state “between life and death”

• Coma is an unconscious state in which the body seems to switch to “autonomous mode”: it maintains basic processes like breathing and heartbeat, but does not respond to external stimuli.

• The causes of coma are different: it can occur due to a serious traumatic brain injury, poisoning, stroke, metabolic failure.

• An artificial coma is a drug-induced sleep that a person is put into with severe damage to the body to help recovery.

• The deeper the coma and the longer a person stays in it, the less likely it is to get out of it – although the state itself can last for years.

• The prognosis for recovery depends on the depth and duration of the coma. After a few hours, the chances of a full recovery are high. But after several weeks with no sign of consciousness awakening, the chances are slim.

The word “coma” in Greek means “deep sleep”. A person in this state really seems to be asleep. But he can’t be awakened, and he (most likely) doesn’t dream. During sleep, a person only seems to be “turned off”. All his systems – breathing, blood circulation, thermoregulation – work normally. During a coma, their mismatch occurs. This is emergency mode.

This condition is based on two mechanisms. The first is a bilateral lesion of the cerebral cortex, which is responsible for higher nervous activity. The second is the defeat of the brain stem in that part of it that is responsible for the activation of the cerebral cortex and reflex activity. These mechanisms can work both separately and together.

In case of violation, there is a failure in the transmission of nerve impulses between brain cells, the coordination between the activity of different structures is lost. As a result, the brain loses its managerial functions. It turns on, as it were, an autonomous mode: a person loses control over his actions.

The normal functioning of consciousness requires the coherence of all systems and the uninterrupted supply of resources for the brain. A sharp and severe lack of certain substances (electrolytes, glucose, oxygen), poisoning with poisons that depress the nervous system (organophosphorus compounds, barbiturates, alcohol), internal waste products can lead to coma.

Among the most common causes of such disorders are overdose of strong drugs or drugs (40% of cases), stroke (about 20% of all cases), cardiac arrest (25%). The rest are metabolic disorders (hypoglycemic, thyrotoxic, hepatic), inflammatory diseases of the brain (encephalitis, meningitis), severe infectious diseases and injuries. In total, several hundred individual conditions are known that can lead to coma.

From minutes to decades. There are examples when several generations of relatives looked after people in a coma. For example, an American woman, Edward O’Bara, fell into this condition at the age of 16 due to complications caused by severe pneumonia due to diabetes. She lived another 42 years and died without regaining consciousness.

The prognosis depends on the causes of the coma, the severity of the impairment, the dynamics of the person’s condition and medical care. The deeper the coma and the more time passes without changes, the less chance of a good outcome. If consciousness is not restored within the first two to four weeks, doctors diagnose a chronic coma. Also, a person can go into a vegetative state (when the cycle of sleep and wakefulness is started, the person feels pain, but there are no signs of consciousness) or a state of minimal consciousness (when the person unconsciously reacts to the environment).

There are very few cases when the patient came to his senses after spending a year or more in a coma. Those who do succeed usually show some positive dynamics in the process: they have reactions to the outside world, they can open their eyes. One of the reliable indicators is the level of brain activity. For example, those patients who have recorded more than 42% of normal brain activity are more likely to come to their senses during the first year.

Depends on the severity of the condition. In a deep coma, a person does not show normal reflex reactions, does not respond to pain, light or sound in the usual way, does not perform voluntary actions, and breathing is confused. It will not be possible to establish contact with such a patient. But there is evidence that in a vegetative state, people can respond to speech addressed to them.

In 2011, neuroscientists used functional magnetic resonance imaging to observe brain activity in a man who had been in a coma for 12 years after a traffic accident. When they asked him to imagine that he was playing tennis or walking in the park, activity in the motor area of ​​his brain indicated that he could respond to the command.

Studies have also shown that the presence of relatives and friends, communication, stimulation of various senses can help a person recover. In January 2015, American physicians published data from a study demonstrating that patients in a coma recovered faster and better than others in the same condition when they listened to recordings of their family members about known family history events through headphones.

Only a doctor can self-diagnose a coma. But by some signs it is possible to determine that it is she: the pupils do not react to light (a sign of inhibition of brain reflexes), there is no reaction to pain (twitches, grimace), breathing is irregular, with long pauses between exhalation and inhalation, arrhythmia, involuntary urination and defecation.

Since coma is not an independent disease, but a concomitant condition, in some cases other symptoms indicate its onset. For example, in diabetes, a coma may be a sudden and severe hunger (indicating a lack of glucose), weakness, dizziness, or thirst and dry mouth (when glucose levels are elevated). With apoplexy coma (due to a stroke), it all starts with a sharp headache, numbness in one half of the body, facial asymmetry.

First make sure it’s not a cardiac arrest by checking breathing and pulse. It is better to call an ambulance right away, even if you suspect that the person has fainted, – this way you will gain valuable time. Before the arrival of the ambulance, lay the victim on his side. In a coma, muscles relax, including the tongue, and it can block the airways.

You can prevent the development of hypoglycemic coma in diabetes – give a person a piece of sugar, candy, a spoonful of jam. If this is not done immediately, drowsiness gradually sets in, gradually turning into depression of consciousness: the person does not respond to external stimuli, the skin turns pale, the pupils dilate, they do not react to light, shallow breathing, the pulse is rare, weak.

Doctors use the terms “sedation” or “medicated sleep”. The purpose of this procedure is to reduce the metabolic rate in the brain tissues. Due to this, brain swelling can be reduced. In addition, in this state, the bioelectrical activity of the brain decreases, a lot of oxygen and glucose are released, which are redirected to maintain cell metabolism in the nervous tissue.

If it is necessary to put a person into such a state, doctors administer special drugs (usually propofol and barbiturates, which depress the functions of the central nervous system). A person’s condition is monitored by specialists in terms of the main parameters – blood gas composition, electrolyte levels, acid-base balance, blood parameters in terms of biochemistry.

An artificial coma is more easily tolerated by the body, but it is still a risk – there may be complications in the form of respiratory tract infections (due to inhibition of the cough reflex), heart problems. Therefore, such intervention is rarely practiced and only in situations where the potential benefits outweigh the risks. Doctors try not to keep the patient on drugs unnecessarily. Most often we are talking about a few days, a maximum of several months.

During a coma, important parts of the brain are practically switched off from the life process. It doesn’t go unnoticed. Due to insufficient blood supply, brain cells can die, partial paralysis can occur, breathing difficulties, and personality changes. Because of the constant stay in the supine position, blood clots may appear in the vessels.

If a person has only been in a coma for a few days, they have a good chance of making a full recovery. But if several weeks or months have passed, the process can be long. Often coordination of movements suffers, a neurosis-like syndrome may occur (when a person becomes irritable or apathetic), there may be problems with memory. Again, it all depends on how serious the root cause was.

Rehabilitation programs may include the introduction of drugs that support metabolism, stabilize blood pressure and temperature, and strengthen the immune system.