Approach to Coma Flashcards
Lethargy?
Sleepy but easily aroused
Hypersomnia?
Excessively sleepy but normal congition when awakened
Obtundation?
Mental blunting, decreased alertness
Stupor?
Eyes open only briefly after vigorous stimulation before returning to deep sleep. Cognition impaired
Coma?
Eyes remain closed after vigorous stimulation
Delirium?
Disoriented, misperception of sensory stimuli, hallucinations. Vacillates between quiet, sleepy periods and hyper-vigilance/agitation
When do pts in comas develop eye opening and sleep wake cycles?
2-4 weeks
Abulia?
Awake but apathetic, no spontaneity. With vigourous stimulation, cognitive function may be normal. (bilateral frontal lobe disease, lobotomized)
Akinetic mutism?
Silent, alert-appearing immobility. No mental activity with vigorous stimulation (disease of frontal lobes and hypothalamus)
Minimally conscious state?
Fragments of awareness
Vegetative state?
Awake, no awareness or meaningful interaction with the enviroment
Patients in MCS may do what?
Reach for objects, grunt, or gesture in response to a command, Visually fixate and track
Components of consciousness?
Arousal, Content
How is arousal achieved?
Neural circuits that mediate sleep-wake cycles and involves a specific area of the upper brainstem referred to as the reticular activating system or ascending arousal system of the rostral brainstem
Disruption of the arousal system leads to?
Stupor and coma
What does the content system refer to?
Cerebral activity for self-awareness, cognition, and purposeful interactions with the environment
Are the content system behaviors premeditative or reflexive in nature?
Premeditative
Lesion in encephalitis lethargica?
Rostral periaqueductal grey matter and posterior 3rd ventricle
Cataplexy?
sudden involuntary loss of muscle tone during emotional excitement
Neuropathological patterns associated with coma?
A. Extensive, acute bihemispheric disease
B. Lesions of the diencephalon (thalamus and hypothalamus)
C. Lesions of midbrain peri-aqueductal grey matter
D-E. Involvement of upper one third of pontine tegmentum
Reticular grey formation?
Mediates arousal
Route of the reticular grey formation?
Upper third of the pons through the midbrain tegmentum, the floor of the third ventricle and into the thalami
Injuries to what will cause coma?
Reticular grey formation
Nuclei responsible for arousal are located where?
Ascending arousal system
What makes up the ascending arousal system?
Two Cholinergic nuclei
Monoaminergic System nuclei
What do the cholinergic nuclei of the AAS do?
Inhibit thalamic firing that increases wakefulness. This puts the thalamus in transmission mode for filtering and relaying sensory info to the cortex.
What happens if you did not have the cholinergic projections to the thalamus?
Thalamus would continue their periodic electrical “bursting” and with their widespread connections to the cortex, induce sleep through synchronizing cortical electrical activity.
Role of the monaminergic system in the AAS?
It has widespread connections to the cortex, both direct and indirect. Improves signal to noise ratio for messages from the thalamus and thereby prevents any misperception of incoming sensory stimuli
What is the sleep promoting center?
The ventro-lateral preoptic nucleus (VLPO)
What NT does VLPO use?
GABA
Role of VLPO?
Inhibits the many nuclear centers that promote wakefulness and comprise the ascending arousal system.
The AAS receives feedback from many sources including?
Thalamus, the Limbic System, the frontal and association cortex
Causes of coma?
Structural, Metabolic, Psychogenic (rare)
What do you always rule out first in a comatose patient?
Psychogenic coma
Structural comas?
Supratentorial mass lesion
Acute obstructive hydrocephalus
Infratentorial mass lesion
Metabolic comas?
Reversible injury (sedative OD) Irreversible injury (hypoxia in cardiac arrest)
What does transtentorial (Uncal) herniation lead to?
Occulomotor entrapment as well as sometimes PCA entrapment.
Common cause of transtentorial (Uncal) herniation?
Epidural hematoma from the laceration of middle meningeal artery
What does a falcine herniation trap?
One of both ACAs
How does a falcine herniation occur?
When mass effect pushes the brain under the falx cerebri
How does central herniation present?
Rostral-Caudal deterioration
- Diencephalon –> midbrain failure
- Reduced conciousness
- Small reactive pupils
- Decorticate posturing
- Cheyne - Stokes respirations
- Midbrain failure follows (FIxed mid-position pupils, decerebration)
Intrinsic brainstem lesions?
Top of the Basilar Artery ischemic stroke
Pontine hemorrhage
Extrinsic brainstem lesions?
Compress and distort the brainstem
- Cerebellar hemorrhage
- Cerebellar infarction
- Cerebellar brain tumor
Primary brainstem lesions?
Segmental cranial nerve deficits
Ascending (spinothalamic) tract dysfunction
Descending (corticospinal, central sympathetic) tract dysfunction
Early cerebellar signs
Pontine hemorrhage presentation?
Abrupt coma Pinpoint pupils Decerebrate rigidity or flaccid quadriplegia Horizontal gaze paresis Ocular bobbing
Metabolic insult to the brain is?
Global, diffuse, symmetric
Neuro-exam shows in pts with metabolic insult?
Does not show any focal or lateralizing deficits
What does head CT show in pts with metabolic insult?
Normal
What is the state of the pupils in metabolic insult?
Reactive
