A coma is a life-threatening state of unconsciousness caused by damage to specific brain structures and characterized by a complete lack of interaction with the surrounding environment. Its causes can be divided into metabolic (poisoning by metabolic byproducts or chemical substances) and organic (resulting in the destruction of brain regions).

The main symptoms are an unconscious state and no eye-opening response even to strong stimuli. Diagnosis relies heavily on CT and MRI scans, as well as blood tests. Treatment focuses primarily on addressing the root cause of the pathological process.

General information

The term “coma” originates from the Greek word for “deep sleep.”

A coma is a type of consciousness disorder where the patient completely lacks interaction with the environment and exhibits no mental activity. This state is so profound that the patient cannot be aroused even with intense stimulation.

In a comatose state, the patient always lies with their eyes closed and does not open them in response to sound or pain, which distinguishes a coma from other types of consciousness disorders. Other signs, such as the presence or absence of spontaneous movements, preserved or diminished reflexes, the ability to breathe independently, or total dependence on life-support devices, depend on the cause of the coma and the extent of nervous system suppression.

Not all severe traumatic brain injuries cause a coma. For a coma to occur, specific areas responsible for wakefulness must be damaged.

Causes of coma

A coma is not a standalone disease but a severe complication of the central nervous system caused by damage to neural pathways. The brain cortex perceives signals from the environment indirectly through the reticular formation. This structure filters and organizes neural impulses. When reticular formation cells are damaged, the brain’s higher regions lose contact with the outside world, leading to a coma.

Damage to the reticular formation’s nerve fibers can occur physically or chemically:

1. Physical Damage: Can result from conditions like a stroke, trauma (gunshot wounds, contusions, hemorrhages).
2. Chemical Damage: Divided into:
   • Internal: Metabolic byproducts formed due to organ diseases, such as low blood oxygen (hypoxia), abnormal glucose or ketone levels (in diabetes), or ammonia (in severe liver diseases).
   • External: Toxins introduced from outside, such as drug overdoses, sedatives, neurotoxic poisons, or bacterial toxins during infections.

A unique damaging factor that combines physical and chemical effects is increased intracranial pressure, which can occur due to traumatic brain injuries or CNS tumors.

Traumatic brain events

Physical trauma to the brain represents one of the most direct paths to coma. Motor vehicle accidents, falls, and other incidents causing severe head injuries can lead to brain swelling, bleeding, or direct tissue damage. The resulting pressure inside the skull disrupts normal brain function, potentially triggering a comatose state.

Metabolic disturbances

Our brain requires precise chemical balance to function. When this balance tips too far in any direction, consciousness can fade. Severe diabetic complications stand out here – both extremely high and low blood sugar can shut down brain function. Similarly, liver or kidney failure allows toxins to accumulate, essentially poisoning the brain into unconsciousness.

Lack of oxygen or blood flow

The brain demands constant oxygen supply. Even brief interruptions can have devastating effects. Cardiac arrest, drowning, carbon monoxide poisoning, or severe asthma attacks can starve the brain of oxygen. Blood clots or hemorrhages block vital blood flow, potentially causing stroke-induced coma.

Infections taking over

When infections reach the brain, whether through direct invasion (meningitis, encephalitis) or as a complication of systemic infection (sepsis), they can cause widespread inflammation and swelling. This inflammatory response, meant to fight infection, can paradoxically shut down brain function.

Toxic exposures

Various substances can push the brain into a comatose state. Drug overdoses, particularly from opioids or sedatives, essentially force the brain to slow down beyond consciousness. Industrial toxins, certain medications, and even severe alcohol intoxication can overwhelm the brain’s ability to maintain awareness.

Brain tumors growing

As tumors grow within the confined space of the skull, they create pressure on surrounding brain tissue. When these masses reach critical size or location, they can compress areas responsible for consciousness or block the flow of cerebrospinal fluid, leading to coma.

The silent threat of medical procedures

Sometimes medical interventions themselves carry risk. Anesthesia complications, though rare, can extend beyond the intended period of unconsciousness. Surgical procedures involving the brain or major blood vessels can occasionally result in unexpected coma.

Recognizing warning signs

Before coma develops, patients often show progressive symptoms: confusion, slurred speech, severe headaches, or unusual behavior patterns. These warning signs, when caught early, can prevent progression to full coma through prompt medical intervention.

Classification

Coma can be classified based on two criteria: the cause and the level of consciousness suppression.

1. By Cause:

   • Traumatic (from brain injuries)
   • Epileptic (a complication of epilepsy)
   • Apoplectic (from a stroke)
   • Meningeal (from meningitis)
   • Tumorous (from brain or skull tumors)
   • Endocrine (from thyroid dysfunction or diabetes)
   • Toxic (from kidney or liver failure)

2. By Severity (Glasgow Coma Scale): Evaluates speech, movement, and eye-opening responses:

   • 15 points: clear consciousness
   • 14–13: mild confusion
   • 12–10: deep confusion
   • 9–8: stupor
   • 7 or less: comatose state

Another classification, mainly used in critical care, divides coma into five stages:

1. Precoma
2. Coma I (stupor)
3. Coma II (stupor)
4. Coma III (atonic)
5. Coma IV (beyond coma)

What happens during a coma?

When the brain experiences severe trauma, toxic exposure, or metabolic disturbance, it begins a cascade of events that can lead to coma.

The process starts in the reticular activating system (RAS), a network of neurons in the brainstem that regulates consciousness. As this system gets compromised, the brain’s normal electrical patterns start to slow down, similar to turning down the dimmer on a light switch.

During the transition into coma, patients often pass through stages of increasing confusion and drowsiness. Their speech may become slurred, their movements uncoordinated, and their responses to the environment progressively slower.

Some individuals report experiencing a sensation of “fading away” or describe their thoughts becoming increasingly foggy before losing consciousness completely.

Once in a comatose state, the brain continues minimal essential functions – breathing, basic reflexes, and certain hormone production – but higher consciousness disappears. Unlike sleep, where dreams occur and external stimuli can trigger awakening, coma represents a deeper state of unconsciousness. The brain shows distinctly different electrical patterns from sleep, with extremely slow waves indicating severely reduced activity.

The body undergoes multiple changes during coma:

• Muscles gradually weaken from lack of use, the digestive system slows dramatically, and the body’s circadian rhythms often become disrupted.
• Blood pressure, heart rate, and breathing patterns may become irregular as the brain’s control centers function at minimal levels.

How does person feel during coma

Recent scientific studies have transformed our understanding of how coma patients process their environment. While these patients show no outward responses – they cannot react to pain, light, or sound in observable ways – research indicates their brains may remain more connected to their surroundings than previously believed.

A 2019 study published in the New England Journal of Medicine by Norton et al. demonstrated that auditory pathways maintain partial function during coma. Their research documented brain responses to environmental sounds like footsteps and voices, even when patients appeared completely unresponsive to external stimuli.

The most significant breakthrough came from Northwestern Medicine in 2015, when researchers led by Dr. Theresa Pape conducted a controlled study examining the impact of familiar voices on comatose patients. Their research, published in Neurorehabilitation and Neural Repair, divided participants into two groups. The experimental group received familiar auditory sensory training (FAST), consisting of recordings of family members sharing stories and memories. The control group experienced only ambient hospital sounds.

Using functional magnetic resonance imaging (fMRI), the team documented remarkable differences between the groups. Patients exposed to family voices showed heightened activity across neural networks compared to the control group. The fMRI scans revealed increased connectivity in regions associated with language processing and consciousness.

A follow-up study by the same team in 2018 reinforced these findings. Published in the Journal of Neuroscience, this research demonstrated that repeated exposure to familiar voices correlated with improved recovery trajectories. The study tracked 40 patients over six months, finding that those who received regular FAST showed significantly better outcomes on standardized consciousness scales.

Symptoms

The hallmark symptoms of a coma are the complete absence of contact with the environment and mental activity. Other clinical manifestations depend on the cause of the brain damage.

1. Body temperature:
   • High temperature (42–43°C) with dry skin: overheating-related coma.
   • Low temperature (32–34°C): alcohol or sedative overdose.
2. Breathing rate:
   • Slow breathing: hypothyroid coma, sedative/narcotic overdose.
   • Deep breaths: coma from severe pneumonia or uncontrolled diabetes.
3. Heart rate and blood pressure:
   • Bradycardia: heart-related comas.
   • Tachycardia and high blood pressure: increased intracranial pressure.
   • Low blood pressure: diabetic coma, sedative overdose, internal bleeding.
4. Skin color:
   • Cherry-red: carbon monoxide poisoning.
   • Cyanosis (blue fingertips/lips): low oxygen in blood.
   • Pale skin: massive blood loss.
5. Responses:
   • Grimaces or reflexive movements: mild coma.
   • No sounds or movements: deep coma.

Diagnosis

A neurologist must determine the cause of the coma and distinguish it from other similar conditions. Witness accounts, patient history, and external signs help identify potential causes. Tests like CT, MRI, and blood analyses are crucial for accurate diagnosis.

Differentiation involves examining eye-opening responses to sound and pain. If the patient does not open their eyes despite stimulation, the state is deemed comatose. Reflex assessments and pupil reactions to light help locate brain damage and confirm the diagnosis.

Particular attention should be paid to the patient’s posture.

A head thrown back with increased neck muscle tone indicates irritation of the meninges, which occurs during hemorrhages or meningitis.

Convulsions affecting the whole body or specific muscles may manifest if the coma is caused by epileptic status or eclampsia (in pregnant women).

Flaccid paralysis of the limbs indicates a stroke, while a complete absence of reflexes suggests severe damage to a large area of the cerebral cortex and spinal cord.

The most critical aspect of differentiating a coma from other states of impaired consciousness is assessing the patient’s ability to open their eyes in response to auditory or painful stimuli. If the reaction to sound and pain results in voluntary eye-opening, it is not a coma. If, despite all efforts, the patient does not open their eyes, the condition is considered comatose.

The pupillary reaction to light is studied meticulously. Its characteristics not only help determine the likely location of the brain lesion but also indirectly indicate the cause of the comatose state. Additionally, the pupillary reflex serves as a reliable prognostic indicator.

Narrow pupils (“pinpoint pupils”) that do not respond to light are typical of alcohol or drug poisoning. Unequal pupil sizes in the left and right eyes indicate increased intracranial pressure. Dilated pupils suggest midbrain damage. Bilateral pupil dilation combined with a complete lack of light response is characteristic of a terminal coma and is an extremely unfavorable sign, indicating imminent brain death.

The Glasgow coma scale (GCS)

The Glasgow Coma Scale (GCS), developed at the University of Glasgow by Graham Teasdale and Bryan Jennett in 1974, provides medical professionals with a standardized method to assess consciousness levels in patients with brain injuries or altered mental states.

Components and scoring

Eye Opening (E): Maximum 4 points

4 points – Spontaneous eye opening

• Patient opens eyes without any stimulation
• ndicates functioning brainstem arousal mechanisms

3 points – Eye opening to verbal command

• Patient opens eyes when asked
• Shows some preserved awareness of environment

2 points – Eye opening to pain

• Eyes open only when receiving painful stimulus
• Indicates deeper level of consciousness depression

1 point – No eye opening

• No response even to painful stimuli
• Suggests severe brainstem dysfunction

Verbal Response (V): Maximum 5 points

5 points – Oriented

• Patient knows person, place, time, and situation
• Indicates intact cognitive function

4 points – Confused conversation

• Patient responds but appears disoriented
• May show signs of post-traumatic amnesia

3 points – Inappropriate words

• Random or exclamatory words
• No sustained conversational exchange

2 points – Incomprehensible sounds

• Moaning, groaning
• No recognizable words

1 point – No verbal response

• Complete absence of any sounds
• May indicate severe brain dysfunction or mechanical impediment

Motor Response (M): Maximum 6 points

6 points – Obeys commands

• Follows simple instructions
• Shows intact motor pathways

5 points – Localizes pain

• Moves purposefully toward painful stimulus
• Indicates preserved sensory processing

4 points – Withdrawal from pain

• Pulls away from painful stimulus
• Basic protective reflexes intact

3 points – Abnormal flexion (decorticate)

• Arms bend, wrists flex, legs extend
• Indicates severe brain dysfunction

2 points – Extension (decerebrate)

• Arms and legs extend
• Shows profound brain dysfunction

1 point – No motor response

• Complete absence of movement
• Worst possible motor score

Clinical application

Initial Assessment:

• Record each component separately (E+V+M)
• Calculate total score (range 3-15)
• Document time of assessment
• Note any factors affecting scoring (intubation, facial trauma)

Serial Monitoring:

• Perform regular assessments
• Track changes over time
• Document trends in neurological status
• Adjust treatment based on changes

Interpretation guidelines

13-15: Mild brain injury

• Generally good prognosis
• May require observation
• Usually preserve memory of event

9-12: Moderate brain injury

• Requires close monitoring
• May need neuroimaging
• Variable outcomes

3-8: Severe brain injury

• Medical emergency
• Often needs intubation
• High risk of poor outcome

Limitations and considerations

Confounding Factors:

• Alcohol or drug intoxication
• Sedative medications
• Language barriers
• Physical restrictions (intubation)
• Facial/orbital trauma

Documentation requirements:

• Individual component scores
• Total score
• Time of assessment
• Relevant limitations
• Response to stimuli type
• Symmetry of responses
• Any unusual findings

Prognostic value

Early stage:

• Initial GCS correlates with outcome
• Serial scores more valuable than single reading
• Rapid deterioration requires immediate action

Long Term:

• Combined with age and other factors
• Helps predict recovery potential
• Guides rehabilitation planning

Other methods of coma diagnostics

Computed tomography

Computed tomography (CT) or magnetic resonance imaging (MRI) of the brain allows for the identification of structural changes in the brain, the presence of masses, and signs of increased intracranial pressure. Treatment decisions—whether conservative or requiring urgent surgery—are made based on the imaging results.

If CT or MRI is unavailable, the patient should undergo X-rays of the skull and spine in multiple projections.

Biochemical blood analysis helps confirm or rule out metabolic causes of the comatose state. Emergency tests are conducted to measure glucose, urea, and blood ammonia levels, as well as to evaluate blood gas ratios and key electrolytes (potassium, sodium, chloride ions).

If CT and MRI results show no CNS abnormalities capable of inducing a coma, further blood tests are performed to detect hormones (insulin, adrenal hormones, thyroid hormones), toxic substances (drugs, sedatives, antidepressants), and bacterial cultures.

Electroencephalography (EEG) is a crucial test for differentiating types of comas. EEG records the brain’s electrical potentials, whose evaluation helps distinguish comas caused by brain tumors, hemorrhages, or poisoning.

Coma treatment

Coma treatment should focus on two main goals:

1. Maintaining vital functions and preventing brain death.
2. Addressing the underlying cause of the condition.

Supporting vital functions begins in the ambulance en route to the hospital and is provided to all comatose patients even before diagnostic results are obtained. This includes:

• ensuring airway patency (realigning a retracted tongue, clearing the mouth and nasal cavities of vomit, using an oxygen mask, or inserting a breathing tube);
• maintaining normal circulation (administering antiarrhythmic drugs, blood pressure-stabilizing medications, or performing closed-chest heart massage).

In the intensive care unit, mechanical ventilation is initiated if necessary.

Anticonvulsants are administered if seizures occur, glucose is infused intravenously, body temperature is normalized (with warming measures for hypothermia or fever management), and gastric lavage is performed in cases of suspected drug poisoning.

The second stage of treatment is carried out after detailed diagnostics, and the medical strategy depends on the underlying cause of the coma. For trauma, brain tumors, or intracranial hematomas, urgent surgical intervention is required.

In cases of diabetic coma, blood sugar and insulin levels are regulated. If kidney failure is the cause, hemodialysis is prescribed.

Prognosis

The first 24-48 hours often determine survival rates. As coma extends beyond two weeks, the probability of full recovery decreases. After 4 weeks, patients who haven’t shown signs of improvement face higher risks of permanent disability or remaining in a vegetative state. Medical literature evaluates a patient’s chances of recovery from a comatose state as follows:

• Precoma or Coma I: Favorable, with the possibility of full recovery without residual effects.
• Coma II and III: Uncertain, with outcomes ranging from recovery to death.
• Coma IV: Unfavorable, with most cases resulting in patient death.

Impact of different causes

Metabolic Comas:
When caused by diabetes, liver failure, or severe infections, these comas often show better recovery rates once the underlying condition receives treatment. Patients frequently regain consciousness within days after metabolic balance restoration.

Traumatic Brain Injuries:
Recovery varies dramatically based on injury severity and location. Younger patients typically show better outcomes. Initial Glasgow Coma Scale scores strongly predict recovery – scores above 8 indicate better chances for meaningful recovery.

Toxic Causes:
Drug overdoses or poisoning-induced comas generally show favorable outcomes after toxin clearance, assuming no permanent brain damage occurred during the exposure period.

Age influence

Younger patients (under 50) demonstrate higher recovery rates and better functional outcomes. This relates to greater brain plasticity and stronger overall physical condition. Children particularly show remarkable recovery potential, even from prolonged comas.

Physical signs that predict outcomes

Brainstem Reflexes:
Preserved pupillary responses and gag reflexes suggest better prognosis. Absent brainstem reflexes often indicate poor outcomes.

Motor Responses:
Any purposeful movement, even slight, suggests higher recovery chances. Complete lack of motor response after painful stimuli indicates worse prognosis.

EEG Patterns:
Certain brain wave patterns predict better outcomes. Complete electrical silence typically indicates poor prognosis, while preserved electrical activity suggests recovery potential.

Coma recovery patterns

When improvement occurs, it typically follows a sequence:

1. Opening eyes spontaneously
2. Regaining sleep-wake cycles
3. Following simple commands
4. Recovering speech
5. Regaining complex functions

Even after awakening, patients often face:

• Physical weakness requiring rehabilitation
• Cognitive deficits needing therapy
• Emotional and behavioral changes
• Memory gaps around the coma period
• Need for long-term support services

Medical complications

Extended coma increases risks of:

• Pneumonia from immobility
• Blood clots
• Pressure ulcers
• Muscle wasting
• Joint contractures.