Neuro ICU > Disorders of Consciousness
Disorders of Consciousness (DoC)
Characteristic Clinical Features of DoC
| Disorder | Arousal & Attention | Cognition | Receptive Language | Expressive Language | Visuoperception | Motor Function |
|---|---|---|---|---|---|---|
| Coma | No sleep-wake cycles* | None | None | None | None | Primitive reflexes only |
| Vegetative State (VS) | Intermittent periods of wakefulness* | None | None | None | Inconsistent visual startle | Involuntary movement only |
| Minimally Conscious State (MCS) | Intermittent periods of wakefulness | Inconsistent but clear-cut behavioral signs of self-awareness or environmental awareness | Inconsistent one-step command-following* | Aspontaneous and limited to single words or short phrases* | Visual pursuit* Object recognition* | Localization to noxious stimuli* Object manipulation* Automatic movement sequences* |
| Post-traumatic confusional state | Extended periods of wakefulness | Confused and disoriented* | Consistent one-step command following | Sentence-level speech, often confused, perseverative. Reliable yes-no responses* | Object recognition | Functional use of common objects* |
| Locked-in syndrome (*not a DoC) |
Normal sleep-wake cycles | Normal to near-normal | Normal | Aphonic | Normal | Tetraplegia |
| *Key distinguishing feature Adapted from Giacino et al. (2014). Nature Reviews Neurology, 10(2), p. 3. doi: 10.1038/nrneurol.2013.279. |
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Complete loss of spontaneous/stimulus-induced arousal; self-limiting, can resolve into either vegetative or MCS.
Eyes remain closed and the patient cannot be aroused
Coma Duration: Important predictor of functional recovery in terms of post-traumatic amnesia (PTA) – a permanent gap of memory from the time of the injury until when the patient starts remembering events.
The severity of the injury is classified:
PTA < 1 hours = mild brain injury
PTA 1-24 hours = moderate brain injury
PTA 1-7 days = severe brain injury
PTA > 7 days = very severe brain injury
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Complete absence of behavioral evidence for awareness of self and environment, but preserved ability for spontaneous or stimuli-induced arousal. Wakeful unconsciousness. Spontaneous eye-opening; the continued absence of language comprehension, any communication, or reproducible/purposeful behaviors in response to stimuli.
Persistent VS: above presentation for > 1 month (28 days)
Permanent/Chronic VS: VS lasting at least 3 months after non-TBI; or 12 months after TBI
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Minimal but definite evidence of self/environmental awareness. Hallmark feature is the inconsistency of these behaviors between exams. Reproducible evidence:
Simple command following
Yes/no comprehension
Language (verbal or gestural)
Non-reflexive behaviors selectively triggered by specific stimuli (i.e., smiling/crying in response to appropriate stimuli, sustained visual pursuit, reaching, manual manipulation of objects with hands)
MCS +: evidence of language comprehension and/or expression
MCS -: skills of consciousness that do not include evidence of any language function
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Acute confusional state; re-emergence of functional communication (reliable yes/no responses concerning personal or situational questions) or meaningful use of objects (hair or toothbrush)
Temporal and spatial disorientation, distractibility, anterograde amnesia, impaired judgment, perceptual disturbance, restlessness, sleep disorder, emotional lability.
Diagnostic Challenge
There is no "gold standard" for detecting conscious awareness — diagnostic error is common. 30–40% of patients diagnosed as vegetative state (VS) actually demonstrate conscious awareness on more rigorous assessment. This can lead to inappropriate medical management, including inadequate pain control. Patient-specific factors such as sensory deficits, seizure activity, or sedating medications may mask conscious awareness and must be considered before concluding a patient is unaware.
Always use a validated standardized tool to assess consciousness level and track changes over time. See Coma Recovery Scale – Revised (CRS-R), Coma/Near Coma Scale, and Rancho Los Amigos Scale – Revised. GCS and RASS scoring are also reviewed on this site.
Potential Patient Presentation and Precautions
(Hamby, 2017; Knight & Decker, 2022)
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Uncontrolled fever often seen following TBI (can also occur following CVA). Generally, diagnosis of exclusion.
Defer therapy if the patient’s temperature >100.9°F, especially in light of other autonomic abnormalities such as bradycardia, lower respiration rate, increased perspiration, and decreased level of consciousness.
Higher mortality rates and increased functional and cognitive disabilities are associated in patients with SAH and fevers > 100.9°F that persist for > 7 days.
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Usually noted in very low-level comatose patients (Rancho Level IV) whose ANS is overstimulated. If new, defer therapy until etiology (e.g., sepsis, MI) has been determined.
Symptoms:
Tachycardia (HR > 130 bpm)
Tachypnea (>40 respirations/min)
Hypertension (extremely high)
Profuse sweating
Extensor posturing
Dilated pupils
Fever (> 101.3° F)
Triggers
Medical causes: urinary retention, infection, pain, dehydration, hydrocephalus
Environmental causes and/or noxious stimulation: such as endotracheal suctioning or loud environment
What Should You Do?
Investigate for/remove noxious stimulus
Assess the need reposition your patient for comfort
Assess the need to make environmental modifications
Monitor vitals and symptoms
Pharmacologic Management
Sedatives (Propofol)
Opioid receptor agonist (Morphine, Fentanyl)
Beta Blockers (Propranolol)
Benzodiazepines (Diazepam) for those with opioid tolerance
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Hypotension (systolic <90mmHg) and hypoxemia (SaO2 <90% or PaO2 <60 mmHg) should be avoided due to the high risk of secondary neurological insults after TBI
These same thresholds apply to activity decision-making — see the TBI Activity Decision Framework for guidance on deferring or stopping therapy when these parameters are not met.
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Risk factors include: GCS of <10, cortical contusion, depressed skull fracture, SDH, epidural hematoma, intracerebral hematoma, penetrating head wound, or seizure within 24 hours of injury.
Defer therapy during active seizure activity. Resume only after the seizure has fully resolved, the patient has returned to baseline, and the medical team has been notified.
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Abnormal posturing is an ominous sign. Only 37% of decorticate and 10% of decerebrate patients survive head injury
Factors that favor survival in TBI with decerebrate posturing include: younger patient age, admission within 6 hours of injury, and extradural hematoma.
Negative outcomes are more associated with acute subdural hematoma and older age
Decerebrate Posturing
Decerebrate posturing can be seen in patients with large bilateral forebrain lesions or caused by a posterior fossa lesion compressing the midbrain or rostral pons. This posturing can also be caused by reversible metabolic disturbances such as hypoglycemia and hepatic encephalopathy. Studies have shown that the vestibulospinal tract plays a major role in decerebrate posturing. In more basic description, the vestibulospinal pathways have an excitatory effect on extensor motor neurons in the spine, while inhibition of flexor motor neurons. Decerebrate posturing results from a disconnection between the modulatory higher centers and the vestibular nuclei (which typically inhibit and prevent the reflex), resulting in unsuppressed extensor posturing.
Described as adduction and internal rotation of the shoulder, extension at the elbows with pronation of the forearm, and flexion of the fingers. As with decorticate posturing, the lower limbs show extension and internal rotation at the hip, with the extension of the knee and plantar flexion of the feet. Toes are typically abducted and hyperextended.
Decorticate Posturing
The mechanism for decorticate posturing is not as well studied as that of decerebrate. Extensive lesions involving the forebrain, diencephalon, or rostral midbrain are known to cause decorticate posturing. This includes the motor cortex, premotor cortex, corona radiata, internal capsule, and thalamus.
Described as abnormal flexion of the arms with the extension of the legs. Specifically, it involves slow flexion of the elbow, wrist, and fingers with adduction and internal rotation at the shoulder. The lower limbs show extension and internal rotation at the hip, with the extension of the knee and plantar flexion of the feet. Toes are typically abducted and hyperextended
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Medical Factors
Psychoactive medications
Paralytics
General anesthesia within 24 hours
Ictal event within 24 hours
Fever >99 within 2 hours of exam
Infectious cause requiring treatment
Known Performance Impairments
Motor impairment (paralysis, spasticity) or physical injury (fracture)
Cranial nerve, visual or perceptual deficits
Other sensory impairment (tactile processing, hearing impairment)
Aphasia
Apraxia
Other
Primary language barrier
Logistical problems or interruptions
⚠ Defer Therapy During Active Storming Episodes
If the patient is in an active autonomic storming episode, stop or defer therapy. Remove or reduce noxious stimuli, ensure the patient is repositioned comfortably, and notify nursing. Resume only after the episode resolves and vitals stabilize. If storming is new and etiology is unknown, defer until cleared by the medical team.
Therapy Implications
(Padilla & Domina, 2016)
Use a validated, systematic approach to assessment and treatment — the CRS-R should anchor both initial evaluation and ongoing tracking to detect subtle changes in consciousness level.
Evaluation of a patient with DoC is focused on identifying subtle behavioral signs in response to sensory stimulation. A standard evaluation of body functions should be performed alongside careful observation of changes in vital signs during task performance.
To assess activation of the reticular activating system: increase the patient's upright position or sit the patient at the edge of the bed with a 2-person assist.
Abnormal posturing is frequently observed in comatose patients and indicates abnormal reflexive activity at the brainstem level. Most commonly seen: decorticate or decerebrate posturing. (See TBI page for full clinical description.)
Research supports bimodal (auditory + tactile) or multimodal (all five senses) strategies to impact attention and cognition. Multimodal cues paired with action/initiation cues may increase level of consciousness and environmental awareness.
Sensory Stimulation Frequency
Start sensory stimulation early and frequently — target 3–5 sessions per day, 20 minutes each, until the patient can participate in more complex tasks. Determine which sensory modality the patient responds to best and use it to facilitate arousal at the start of each session.
Treatment/Sensory Stimulation
(Cluck & Otr, 2015)
Use the Coma Recovery Scale-Revised (CRS-R) to track progress and guide treatment across sessions.
Early treatment focus: sensory stimulation, neuro re-education, and prevention of contracture and confounders through ROM, positioning, and mobilization.
For OT, the initial focus is preparatory — progressing to ADL participation as consciousness level improves.
Goals of sensory stimulation:
Increase arousal and attention to allow the patient to perceive incoming stimuli
Improve the quantity and quality of responses
Provide opportunities for the patient to respond to the environment
Heighten responses to sensory stimuli and channel them toward meaningful activity
Goals for the Low-Level Coma Patient at Rancho Level I-III
(Hamby, 2017)
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Patient will open their eyes for 10 seconds with verbal stimulation
Patient will grasp ADL item (washcloth, comb, toothbrush) for 10 seconds when placed in their hand
Patient will sustain arousal for 1 minute during a task
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Patient will respond to 50% of simple 1-step commands
Patient will follow verbal commands to wash face
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Patient will maintain visual attention to and/or track a photo of familiar family member/friend or personal item for 10 seconds
Patient will maintain visual attention to a grooming item for 10 seconds
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Patient will attend to or turn head to auditory stimuli
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Patient will tolerate sitting edge of bed for 5 minutes to participate in simple ADL task with 2 person assist
Patient will maintain trunk in midline position in bed or chair position while performing simple grooming task for 5 minutes with supervision
DoC & Cognitive Recovery (Rancho Level 1-3)
Informative video with treatment visuals from Craig Hospital
References
Cluck, J., & Otr, M. M. (2015, June 29). Activities for stimulation of persons with low arousal. http://s3.amazonaws.com/arena-attachments/715662/060c23188c291627d8f659d068607996.pdf?1474669884
Giacino, J. T., Fins, J. J., Laureys, S., & Schiff, N. D. (2014). Disorders of consciousness after acquired brain injury: The state of the science. Nature Reviews Neurology, 10(2), 99–114. https://doi.org/10.1038/nrneurol.2013.279
Hamby, J. (2017). The Nervous System. In H. Smith-Gabai & S. E. Holm (Eds.), Occupational Therapy in Acute Care (2nd ed.). AOTA Press. https://library.aota.org/OT_in_Acute_Care_2e/134?highlightText=intensive%20care%20unit
Knight, J., & Decker, L. C. (2022). Decerebrate And Decorticate Posturing. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK559135/
Padilla, R., & Domina, A. (2016). Effectiveness of sensory stimulation to improve arousal and alertness of people in a coma or persistent vegetative state after traumatic brain injury: A systematic review. The American Journal of Occupational Therapy, 70(3), 7003180030p1-7003180030p8. https://doi.org/10.5014/ajot.2016.021022

