3 - Reticular System Flashcards
Reticular System:
Definition
Target
Diffuse collection of >110 nuclei; extends from medulla to the forebrain
Projectiosn to thalamus and cortex
What does the Reticular System intregrate?
Integrates information from all senses (EXCEPT OLFACTION) to modulate brain functions
Ex: Pain, Motivation, Respiration, Sleep, REM sleep
Ascending Reticular Activating System (ARAS)
Consciousness, Arousal, Attenion, Wakefullness
Allows purposeful interaction with your environment
Reticular Formation Divisions: Rostral vs Caudal
Rostral: Supplies cerebral cortex with excitatory inputrs for consciousness/wakefullness/arousal/attening (ARAS SYSTEM)
Caudal: Modulates motor function via medial and lateral reticulospinal tracts (descending tracts)
Major Functions of the Ascending Reticular Activating System (ARAS)
Prime
Filter
Shunt
Primes - the corect and othe rbrain regions allowing incoming sensory information to be proessed (focuses attention)
Filters - out information that is unimportant
Shunts - information that is life-threatening or fearful directly to amygdala
Reticular Formation Divisions: Telencephalon
Nucleus Basalis of Meynert
Major source of cholinergic (ACh) neurons for the cortex and amygdala (w/out thalamic relay)
Clinical: Substantial neurodegeneration is always associated with cognitive dysfunction, decline, dementia, AD
Reticular Formation Divisions: Diencephalon
Reticular Nucleus of the Thalamus
Wide variety of thalamic and hypothalamic nuclei strongly associated with reticular formation
Retocular Nucleus of the Thalamus: Only thalamic nuclei to have no projections outside of the thalamus
Integrates incoming information from cortex, thalamic relay and other ARAS inputs; may control when information is sent to various cortical areas
Telencephalon - Nucleus Basalis of Meynert
Major source of Cholinergic (ACh) Neurons for cortex and amygdala (without thalamic relay)
Degeneration can be associated with cognitive dysfunction, dementia, AD
Diencephalon - Reticular Nucleus of the Thalamus
Only thalamic nuclei to have no projections outside the thalamus
Integrates information incoming from cortex, relay, and other ARAS inputs
May control when information is sent to various areas (coordination role)
Midbrain Pathways
Two (PAG, Dorsal Raphe Nucleus) main pathways that carry nociceptive signal to somatosensory cortex with collateral going to reticular formation
Midbrain - Periaqueductal Gray (PAG)
Modulation of descending pain transmission
Determines whether pain will be transmitted; contains high desnity of Opiod receptors
MIdbrain - Dorsal Raphe Nucleus
Primary site of serotonergic neurons (5HT) in reticular formation
Modulates pain transmission; no thalamic relay
Modulates consciousness, attention, and mood (ARAS)
Midbrain - Ventral Tegental Area (VTA)
Mesolimbic (DA) and mesocortical pathways
Critical in reward circuitry, memory, attention, and motivation
Midbrain - Substantia NIgra Pars Compacta (SNc)
Nigrostriatal (DA) pathways; modulation of basal ganglia
Parkinson’s Disease
Pons - Nucleus Locus Coeruleus (blue nucleus)
Majority of Norepinephrine (NE) input in CNS
Ascending / Descending projections to the limbic structures, dorsal horn, and cortex (without relaying in the thalamus)
Modulates ARAS - arousal, selective attention, stress response, pain modulation, and mood
Clinical: Degenerates in both AD / Parkinsons
Pons - Pedunculopontine Nucleus and Lateraldorsal Tegmental Nucleus
Largest sites of Acetylcholine (ACh) production in brain
Involved in ARAS / REM sleep; part of indirect arousal system
**Must be inhibited for sleep to occur**
Medulla - Nucleus Raphe Magnus (5HT) and Rostral Ventral Medulla (RVM-Glutamate)
Regulate whether information will be transmitted higher in the brain; modulates transmission of pain to the dorsal horn
Medulla - Nuclei of the Medullary Reticular Formation
- Critical in vital functions; cardiovascular and respiratory center regulation
- Death can occur from tonsillar herniation compression of these structions
- Opiod abuse results in depression of respiratory centers
- SIDS possibly factor here
How does the ARAS Prime?
Focuses attention, increase general alertness
How does the ARAS filter?
Bottom-Up control; removes conscious awareness of information perceivd to be unimportant
Modulates how information is represented to the cortex
How does the ARAS shunt?
Sends information that is life-threatening or fearful directly to the amygdala
Where are major ARAS nuclei clustered?
Ponto-mesencephalic diencephalic regions of reticular formation
ARAS facilitated learning
ARAS ACTIVATES the cortex (entorhinal/hippocampus)
Cortex tells ARAS what is important allowing filtering of extraneous information
Memory formed
Clinical: Amnestic Agent
ARAS Depression produces state of unconsciousness; still allows activity in the thalamic and cortical areas, but there will be no arousal = NO formation of memory
Ex. Midazolam (Versad)`
Clinical: Bilateral lesion of Ponto-mesencephalic-diencephalic region of Reticular Formation?
Critical for maintaining consciousness
Bilateral Lesion = Coma
What are the two pathways of consciousness?
Direct - Aminergic Contributions
- Direct Cortical Projections (no Thalamic relay)
- Activated only during waking state/regulating overall activity of the brain
- - -
Indirect - Cholinergic Contributions
- Indirect projection to cortex VIA thalamic relay
- Activated during waking state and REM sleep
What are the two parts of consciousness?
Content and Level
Content: Sensory, Motor, Memory, Emotion
Level: Attention, Alertness, Awareness
One side can not maintain consciousness alone!
Clinical: Bilateral lesion of upper brainstem affecting ARAS nuclei and pathways, or bilateral thalamic lesion?
Loss of consciousness
Clinical: Bilateral compromis or destruction of the hemispheres?
Causes?
Toxic insult, metabolic, anoxia, drug or alcohol overdose, barbiturates, encephalopathy/increased brain pressure
Clinical: Focal or Unilateral lesion of the thalamus (as long as the RAS projectings to at least one hemisphere and thalamus are intact)
Generally–do not generate coma directly, but can indirectly via tonsillar herniation
Clinical: Locked in Syndrome
Bilateral Ventral Pontine Lesion
Prevents Corticospinal (trunk/limb) / Corticobulbar (non-oculomotor face, head, neck) motor output
Symptoms: Quadriplegia, Aphonia (can’t speak)
Preserved: ARAS is unaffected = fully conscious, sensory function, vertical eye movement, and blinking
Clinical: Akinetic Mutism, Abulia, Catatonia
Distinct constellationof psychomotor disturbances; bilateral medial frontal lobe lesion with intact ARAS
Symptoms: Apathy, Deficits in response initiation, No spontaneous movement, Purposeful response some aversive stimuli, intact reflexes, normal sleep wake cycles
Staring, Mutism, Refusal to eat, abnormal posture, grimace
Clinical: Minimally Conscious State
Impaired function of cortex and ARAS due to widespread cerebral damage
Cause: Diffuse cerebral hypoxia or trauma
Symptoms: Periods of responsiveness or wakefullness with minimal and variable awareness, visual tracking intact, sleep/wake cycle intact, highly variable EEG
Clinical: Vegetative State
> Month = Persistent vegetative state
Severe impaired cortical function; some ARAS may be preserved
Symptoms: Periods of wakefulness, no period of awareness; NO visual tracking, may react to pain
- Small number of patients can activate parts of brain by thinking of an activity; return of visual tracking may indicate + sign patient is recovering
Clinical: Coma
Severe impairment of cortical function and ARAS; prolonged loss of consciousness
Symptoms: Unresponsive, no reaction to sensory input, no awareness, no sleep wake cycle, som primitive reflex activity is present
Clinical: Brain Death
All cortical, subcortical, brainstem function is lost
Only spinal cord function may be preserved
What occurs if the reticular system does not prime an area to receive information?
The sensory information will not be processed
