Disorders of Consciousness (DoC)
Frequent sequel of TBI. Measured using GCS and Rancho Los Amigos Cognitive Scale. JFK Coma Recovery Scale and Rappaport Coma/Near Coma Scale in combination with Disability Rating Scale can also be used in the initial evaluation.
Diagnostic Challenge: There is no “gold standard” for detecting conscious awareness and error is common. 30-40% of patients diagnosed in VS actually regain conscious awareness. Can lead to inappropriate medical management (i.e., inadequate pain control). Patient-specific characteristics or underlying impairments may mask conscious awareness (i.e., sensory deficits, seizure activity, or sedating medication).
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Complete loss of spontaneous/stimulus-induced arousal; self-limiting, can resolve into either vegetative or MCS.
Eyes remained 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-TB; 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.
Characteristic Clinical Features of DoC
Note. Adapted from “Disorders of consciousness after acquired brain injury: The state of the science”, by J. T. Giacino et al., 2014, Nature Reviews Neurology, 10(2), p. 3 (doi: 10.1038/nrneurol.2013.279). Copyright 2014.
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 (Propranaolol)
Benzodiazeepines (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
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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
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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
Therapy Implications
(Padilla & Domina, 2016)
It is critical to implement a systematic approach to assessment and treatment
The evaluation of a coma patient is focused on identifying subtle signs in response to sensory stimulation.
A typical evaluation of body functions should be performed along with careful observation of changes in vital signs in response to task performance.
To assess activation of the reticular activating system: increase the patient’s upright position or sit the patient edge of the bed with a 2-person assist.
Abnormal Posturing: frequently observed in the comatose patient. Indicates abnormal reflexive activity at the brainstem level. Most commonly seen is decorticate or decerebrate posturing.
Research suggests that bimodal (i.e., auditory and tactile) or multimodal (i.e., all five senses) strategies impact attention and cognition. Start sensory stimulation early and frequently (i.e., 3-5 times/day for 20-minute sessions), until more complex task participation is possible
*Multimodal cues paired with action/initiation cues may increase the level of consciousness and environmental awareness
Treatment/Sensory Stimulation
(Cluck & Otr, 2015)
Use the Coma Recovery Scale-Revised (CRS-R) to track progress and guide treatment.
The early focus should be: primarily sensory, neuro re-education, and prevention of contracture or confounders through sensory stim, ROM/positioning, and mobilization.
For OT, the initial focus is more preparatory with progression to ADL
Sensory Stimulation: Used to improve arousal and awareness; stimulate neural recovery process to:
Increase arousal and attention to allow the patient to perceive incoming stimuli
Improve quantity and quality of responses
Provide opportunities for patients to respond to the environment
Heighten patient’s responses to sensory stimuli and eventually channel them into meaningful activity
*Determine which sensory stim the patient responds to best and use that to facilitate arousal at the start of treatment.
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 (Racho 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