The Sensorium: Components, Functions and Consciousness

• The Sensorium

Components

• Includes consciousness, attention span, and orientation to time, place, and person
• Consists of fund of information, insight, judgement and planning, and calculation

Functions

• Awareness of self and environment
• Involves registering internal and external contingencies
• Relates current internal and external stimuli to memories, future hopes, and desires
• Afferent stimuli invested with emotion determine significance and assign priority
• Proposes actions and their consequences
• Directs the motor system for survival and satisfaction
• Allows experiences to be processed consciously with past, present, and future considerations

Consciousness

• A state of full awareness of self and environment
• Requires normal responsiveness to external stimuli and inner needs
• Dependent on arousal and awareness elements

Arousal (Wakefulness)

• Integrity relies on the ascending reticular activating system (ARAS)
• ARAS is made up of neurons lying within the tegmentum of the upper half of the brainstem

Awareness (Content)

• Integrity relies on the cerebral cortex
• Quality and coherence of thought and behavior is also necessary

Normal Alertness

• Requires full responsiveness to perception and indication by speech and behavior
• Includes attention to and interaction with immediate surroundings
• Ability to fluctuate during the day from keen alertness to deep concentration
• Ability to shift from inattentiveness to full alertness and mental function quickly

Confusion

• Involves the inability to think with customary speed, clarity, and coherence
• Causes impaired judgement and decision making
• Often due to processes affecting the whole brain like encephalopathies or dementia
• Most events involving a confused patient leave no trace in memory

Confusion Tests

• Recall events, test working memory, serial subtraction or spelling backward, digit span backward, and registration

Sundowning

• The clouded interpretation of internal/external experience
• Inability to integrate and attach symbolic meaning to experience
• Experience is common in dementia
• The degree of confusion varies throughout the day
• Confusion is least pronounced in the morning
• Confusion increases throughout the day and peaks in the early evening

Delirium

• Derived from the Latin term meaning "to go out of the furrow"
• Characterized by severe inattentiveness, altered mental content, hyperactivity, hallucinations, and misperception of sensory stimuli
• Disorientation progressing from time to place and then to persons

Drowsiness

• Involves the inability to sustain a wakeful state without external verbal stimuli
• Involves a degree of inattentiveness and mild confusion that improves with arousal
• Causes decreased mental, speech, and physical activity
• Patient shifts positions naturally without prompting
• Eyelids droop, snoring may occur, and limbs are relaxed

Obtundation

• Derives from the Latin term meaning "to beat against or blunt"
• Defined by mental blunting and a mild to moderate reduction in alertness
• Includes less interest in the environment and slower response to nonpainful physical stimulation

Stupor

• Derives from the Latin term meaning "to be stunned"
• Is a deeper state than drowsiness
• Requires vigorous and repeated painful stimuli to rouse the patient
• Usually requires continued stimulation to sustain arousal
• Responses to spoken commands are absent, curtailed, or slow and inadequate
• Causes a reduction or elimination of natural shifting of positions
• Eyes are displaced slightly out and up

Coma

• Derived from the Greek term meaning "deep sleep or trance"
• Causes incapability of arousal by external stimuli or inner need
• In lighter stages, corneal, pupillary, and pharyngeal reflexes can be elicited
• In the deepest stage, no reactions are obtainable and reflexes are diminished

Persistent Vegetative State

• It is defined by patients recovering from coma only to return to a state of wakefulness without cognition
• Eyes-open permanent unconsciousness characterized by loss of cognitive function and situational awareness
• Preservation of sleep-wake cycles and vegetative function persist in these individuals
• The vegetative syndrome of unconscious awakening persists for 3 months after nontraumatic brain injury
• The vegetative syndrome of unconscious awakening persists for 12 months after traumatic injury
• Anoxia is a key cause
• Ischemia has the worst prognosis
• Other causes include metabolic or encephalitic coma and head trauma
• MRI shows global brain atrophy, thalamic and basal ganglia disproportionately affected
• MRI also shows atrophy of white matter, secondary ventricular enlargement, and thinning of the corpus callosum
• The cortex is diffusely injured or disconnected from the thalamus

Vegetative State (Unresponsive Wakefulness)

• Involves severe cerebral injury leading to coma
• Patients open their eyes in response to pain or spontaneously
• Loss of sphincter control, primitive postural and reflex movement, and automatisms occur
• Respiration may quicken in response to stimulation
• Patients remain unresponsive, do not speak, and show no signs of awareness or purposeful behavior
• EEG shows a lack of normal change in background EEG activity after stimulating the patient
• Neuroimaging shows progressive and profound cerebral atrophy

Brain Death

• State of coma with irreversible brain damage and ceased function
• Pulmonary and cardiac functions can still be maintained by artificial methods
• Complete unresponsiveness to all modes of stimulation, arrest of respiration, and absence of EEG activity for 24 hours is present
• A person is considered dead if the brain is dead even if the heart and lungs are still functioning
• Absence of all cerebral and brainstem functions is not reversible

Brain Death: Complete Absence

• Absence of Cerebral Function Includes a deep coma
• Total lack of spontaneous movement and of motor and vocal responses to all visual, auditory, and cutaneous stimulation
• Absence of Brainstem Function Includes loss of pupillary response
• Loss of corneal, oculocephalic, oculovestibular reflexes, and gag and cough reflex
• Absence of facial movement to noxious stimuli stems from extremities

Brain Death Determinations and Tests

• Etiology of brain injury, history, exam, and neuroimaging must be consistent with irreversible catastrophic injury to the whole brain
• An apnea test tests an individual's destruction of the medulla and unresponsiveness of medullary centers to high carbon dioxide tension
• PaCO2 must be at 60mmHg (normal range is 35-45mmHg) in blood to be determined
• Atropine is given, reflecting loss of cardiac innervation by damaged medullary vagal neurons
• EEG confirms cerebral death through electrocerebral silence, flat or isoelectric EEG
• Absence of contrast opacification during 4VA occurs, resulting in a lack of perfusion in Digital Subtraction Angiography (DSA)
• CTA, MRA, SPECT, and TCD may also be used
• A Toxicologic Screening is used to rule out reversible causes
• Isoelectric EEG with preserved brainstem reflexes may indicate hypothermia
• Intoxication with sedative-hypnotic drugs or recent cardiac arrest can also cause this presentation

Glasgow Coma Scale (GCS)

• Created in 1978 by neurosurgery professors Graham Teasdale and Bryan Jennett at the University of Glasgow
• The scale objectively describes the extent of impaired consciousness in patients
• GCS Aspects of the Glasgow Coma Scale:
• Eye opening
• Verbal response
• Motor response
• Highest score: 15, Lowest score: 3
• Use the Glasgow Coma Scale to check, observe, stimulate, and rate the patient

GCS Details

• Eye Opening (E):
• 4: Opens eyes spontaneously
• 3: Opens eyes to voice
• 2: Opens eyes to pain
• 1: No eye opening
• Best Verbal Response (V):
• 5: Appropriate and oriented
• 4: Confused
• 3: Inappropriate words
• 2: Incomprehensible (moans/groans/sounds)
• 1: No sound
• Best Motor Response (M):
• 6: Obeys commands
• 5: Localizes to pain
• 4: Withdraws to pain (normal flexion)
• 3: Abnormal flexor response
• 2: Abnormal extensor response
• 1: No movement
• NT: Not testable like with intubated patients

GCS Motor Reponses

• The GCS looks for motor responses through finger tip pressure, trapezius pinch, and supraorbital notch
• These responses are classified as:
• Normal flexion with rapid movement away from the body
• Abnormal flexion which is a slow stereotyped movement of arm across chest
• A thumb that is clenched and legs extended
• Decerebrate posture is an abnormal extensor response

GCS-P

• Developed by Paul Brennan, Gordon Murray, and Graham Teasdale in 2018
• A 4th number, the pupil reactivity score (PRS), is subtracted from the standard GCS score

Pupil Reaction Score

Pupil Reaction Score for GCS-P

• 2: Neither pupil reacts to light
• 1: One pupil doesn't react to light
• 0: Both pupils reactive to light
• GCS-P: GCS-(PRS: Range: 1-15

Glasgow Coma Scale for Head Injuries/Traumatic Brain Injury (TBI)

• 13-15 = mild TBI
• 9-12 = moderate TBI
• 3-8 = severe TBI
• With GCS-P: 1-8 = severe

Diagnostic Considerations

• Establish and maintain airway, breathing, and circulation
• Monitor vital signs and manage fluids
• Assess neurologic function and run lab screening
• Initiate specific treatment and obtain a detailed history
• Perform systematic examination and additional diagnostic tests

Neurologic Case Characteristics

• Focal neurologic deficit, increased intracranial pressure (ICP), and meningeal irritation is considered

Neurologic Problems

• Congenital/developmental issues, trauma, infections, degenerative conditions, and metabolic/endocrine disorders
• Nutritional, vascular, demyelinating, immunologic, and neoplastic issues are also considerations
• Disease Categories Mnemonic:
• V: Vascular
• I: Infectious
• N: Neoplastic
• D: Degenerative
• I: Inflammatory/latrogenic/Idiopathic
• C: Congenital
• A: Autoimmune/Allergic
• T: Traumatic
• E: Endocrine/Metabolic

Trauma

• Epidural/subdural/subarachnoid/intracerebral hemorrhage

Infections

• Meningitis, encephalitis, brain abscess

Mass Lesions/Neoplastic

• Neoplasm, abscess, hematoma, granuloma, cyst

Vascular Problems

• Cerebral infarction/hemorrhage/SAH

Type of Lesion

• Focal: Mass lesion, infarction, hematomas
• Multifocal: Multiple tumors, mass lesions
• Diffuse: Metabolic endocrine, toxic encephalopathy

Alterations in Consciousness

• Structural Causes: Discrete lesion, widespread destructive changes of the hemispheres, and increased ICP
• Functional Causes: Metabolic, toxic, nutritional issues resulting from neuronal failure in the Cerebrum and RAS

Structural Causes Specifics

• Secondary Compression of the ARAS: Large mass in one cerebral hemisphere resulting in a tumor, abscess, or massive infarct. Can also be caused by intracerebral, subdural/epidural hemorrhages, or large cerebellar lesion
• Direct Damage to ARAS can be caused by a destructive lesion within the thalamus or midbrain
• Widespread Bilateral Damage to Cortex and Cerebral White Matter - Trauma, bilateral strokes, hemorrhages, encephalitis, meningitis, hypoxia, or global ischemia, and interruption of thalamocortical impulses or generalized destruction of cortical neurons

Head Trauma

• Can cause structural lesions
• Has intracranial complications include:
• Epidural Hemorrhage
• Subdural Hemorrhage
• Subarachnoid Hemorrhage
• Intracerebral Hemorrhage
• Can cause acute subdural hematoma

Cerebrovascular Accident

• Is a structural lesion causing infarction and hemorrhage
• It is an acute condition Infection

Infection

• Is a structural lesion in the brain and can result in meningitis, encephalitis, meningoencephalitis, or an abscess
• Maybe acute, subacute, or chronic
• Meningitis causes inflammation or swelling of layer of meninges tissue surrounding the brain
• Encephalitis inflammation of the brain
• Meningoencephalitis inflammation of both the meninges and the brain

Meningeal Irritation

• Can be acute where there is (+-)fever with Subarachnoid Hemorrhage (SAH)
• (+) fever indicates there is acute meningeal inflammation
• Can be chronic where there is (+) fever and Chronic Meningeal inflammation
• Look for the following:
• Resistance on passive neck flexion indicating nuchal rigidity, which is a neurological problem
• Investigations involve cranial CT scans and CSF examinations

Focal Neurologic Deficits and Cases Specifics

Focal Neurologic Deficits

• Cerebrum: Includes disturbance in higher intellectual functions such as seizure
  • It can also include language problems and personality/behavioral and mental changes
  • Other indicators are contralateral hemiparesis with the babinski sign, contralateral hemisensory deficit and visual field deficit
• Brainstem: Crossed Motor/Sensory Syndrome. This includes contralateral hemiplegia, ipsilateral cranial nerve deficit and a contralateral hemisensory deficit
• Cerebellum: Causes truncal and limb ataxia

Focal Neurologic Deficit

• Can be due to acute conditions like vascular issues, ischemic issues hemorrhagic issues
• Can be due to chronic issues steming from degenerative diesases, mass lesions neosplatic issues, abscesses hematoma
• Also linked to granulomas, cysts, and strokes

Increased Intracranial Pressure

• Acute causes stem from trauma, epidural hematomas, febrile conditions, infections, cerebral infarctions, and parenchymal and subarachnoid hemorrhages, and SAH
• Chronic causes may result pseudotumor cerebr, tumor, dementia, and may require ICP and or incoordination
• Involves running cranial CT scans and MRI
• Chronic menigitis and hydrocephalus are also chronic causes
• Ancillary test needed include the CSF examination test for those with pseudotumor

Meningeal Irritation

Aneurological problem causing infection, which is Meningitis Investigations -Cranial CT scan -CSF examination,

Alteration of Consciousness

• Caused by Structural Lesions, where you rule our MI, increased ICP, and Focal Neurologic Deficit (FND)
• Run cranial imaging and CSF examinations.
• Hemorrhagic complications from trauma, CVA and mass lesions

Causes of Alteration in Consciousness

• Is due to metabolic disorders like glucose related disorders
• It stems diminishes oxygen level decreases and fluid imbalances
• Also results from electrolyte inbalances and excessive accumulation of endogenous waste
• Other issues liek nutritional deficienies and toxicities can also cause the abnormality Alteration of Functional Issues/Deficits
• Stems from Encephalopathy which alters the state of consciousness There are behavioral and personality changes, acute confusional episode and delirium
• Can induce Generalized Seizures
• FND is absent or bilateral

Functional Lesions

• Is found in Encephalopathy and Metabolic-endocrine conditions
• Associated with increased ICP and FND
• Also causes imbalances in nutritional needs

In Alterations of Altered State of Consciousness

• Lesions will stem primary from the spinal and bihimephrial legions that cause herniation syndromes
• Encephalopothy-like symptoms arise and create secondary compressions
• Encephalopothy related symptoms from toxic, metabolic, and hypoxic scenarios