Twenty One Flashcards
Where is the reticular formation? Why are its nuclei impossible to circumscribe? What are 7 general functions of the reticular formation?
The reticular formation is located in the center of the medulla, pons, and midbrain and is surrounded by the various motor, sensory, and visceral nuclei and tracts in the brainstem. It receives input and gives output to all parts of the CNS. Within the reticular formation are numerous nuclei, most of which are indistinct and impossible to circumscribe. In general, the reticular nuclei can be described as forming seven major functional groups: 1) those influencing cranial nerve output, 2) those influencing voluntary movements, 3) those regulating visceral activity via the autonomic nervous system, 4) those participating in the conduction and modulation of slow pain, 4) those associated with the diffuse modulating
systems, 6) those associated with respiration, and 7) those regulating sleep, arousal, and wakefulness.
Where are 4 of the more influential afferent connections to the reticular formation?
Afferent connections to the reticular formation come from many sources. Among the more influential structures are:
Spinal cord - a massive spinoreticular projection that ascends from the anterolateral quadrant of the spinal cord and terminates mainly in the medial part at medullary and
pontine levels.
Cranial nerves - strong input chiefly from the secondary sensory nuclei of the trigeminal, auditory, vestibular, glossopharyngeal, and vagus nerves, as well as a weaker contribution from the optic and olfactory nerves, has been traced into the reticular formation at all levels.
Cerebellum - impulses associated with equilibrium and posture, chiefly from the vestibular part of the cerebellum, project to the reticular formation at medullary levels.
Forebrain - impulses descending from the hypothalamus, the thalamus, and the basal ganglia terminate in the midbrain reticular formation. Impulses from the cerebral cortex, mainly the sensorimotor areas, project to the reticular formation at pontine and medullary levels.
What are some output pathways from the reticular formation?
Efferent fibers from the reticular formation descend to the spinal cord and ascend to the forebrain. The descending influences are mediated via reticulospinal fibers which arise at various levels of the reticular formation.
Ascending projections arise from all levels of the reticular formation and take ventral and dorsal routes. The ventral route includes hypothalamic centers whereas the dorsal route includes centers in the medial part of the thalamus. Both influence widespread areas of the cerebral cortex.
What actions do the reticular formation interneurons help carry out at the levels of the caudal medulla, rostral medulla, pons, and midbrain ?
Cranial nerve output – reticular formation interneurons that regulate cranial nerve output are organized at segmental levels:
caudal medulla: swallowing, coughing, gagging, vomiting, respiration, and cardiovascular reflexes
rostral medulla: equilibrium
pons: facial movements,horizontal gaze, mastication, blinking, auditory reflexes, etc.
midbrain: pupillary, ocular and auditory reflexes
How does the reticular formation influence voluntary movement? What movements? What part of the RF?
Voluntary movements - Impulses descending via the reticulospinal tracts have a strong influence on axial and limb muscles, muscle tone, and myotatic reflexes.
How does the slow pain pathways compare to the fast pain? Where are its nuclei and tracts located comparatively? What aspects of pain does slow pain subserve?
Slow pain conduction - Anatomical and clinical evidence indicates that the fast and slow pain paths are dissimilar. The fast pain associated with pin prick testing is carried by
phylogenetically newer neurons that form the neospinothalamic system. Slow pain, on the other hand, is transmitted by phylogenetically older neurons that form the paleospinothalamic and spinoreticulothalamic systems.
The neospinothalamic neurons subserving fast pain from spinal nerves are located more dorsally in the spinal gray than the slow pain paleo- and spinoreticulothalamic neurons.
Thus, most neospinothalamic neurons are in lamina I, while most paleospinothalamic neurons are in laminae IV, V, and VI. The nociceptive neurons in laminae VII and VIII give rise to the spinoreticulothalamic system.
In the spinal end, the fast and slow pain paths are intermingled in the anterolateral quadrants. However, in the brainstem the fast pain pathway, the spinothalamic tract, is located laterally, whereas the slow pain paths are located medially, that is, in the reticular formation.
Paleospinothalmic fibers have branches that terminate in the reticular formation where they overlap with the terminations of the spinoreticular fibers. These two slow pain inputs to the reticular formation form a massive multipsynaptic spinoreticulothalamic system that projects nociceptive impulses to the medial part of the thalamus. On the other hand, the neospinothalamic tract or fast pain path, projects to the ventroposterolateral nucleus located
in the lateral part of the thalamus. Thus, the lateral thalamus subserves fast pain while the medial thalamus subserves slow pain. The cortical areas receiving nociceptive impulses from the lateral thalamus (VPL and perhaps posterior thalamic nuclei) subserve the sensory-discriminative aspects of pain such as precise localization, sharpness and, intensity, while those areas receiving nociceptive impulses from the medial thalamus (intralaminar and medial nuclei) subserve the arousal, attentional, affective and motivational aspects of pain.
In general, how is slow pain modulated? Which neurons (location/type) are most important? What happens in endogenous modulation? What happens in exogenous modulation? How is exogenous modulation used clinically?
Slow Pain Modulation
The anatomical features of exogenous and endogenous modulation of the spinal pain paths are well-known. In both cases interneurons in the substantia gelatinosa (lamina II) and deeper layers (III, IV, V) of the spinal gray play a key role. These interneurons connect with secondary slow pain neurons in the spinal gray. Through their action the excitability of the secondary slow pain neurons can be altered to prevent their transmission of pain impulses to
higher centers.
Exogenous
Large cutaneous afferent nerve fibers subserving touch, upon being stimulated in massive numbers, are able to modulate pain through connections with substantia gelatinosa and other dorsal horn interneurons. These connections occur via branches of the touch fibers ascending in the dorsal columns. This phenomenon was first suggested by the gate theory of Melzack and Wall. It is currently the basis for the clinical control of chronic pain by transcutaneous electrical nerve stimulation (TENS) in which impulses are selectively elicited in the larger touch fibers.
Endogenous
Groups of neurons in the periaqueductal gray of the rostral midbrain and the periventricular gray of the adjacent diencephalon, upon electrical or neural stimulation, or upon the administration of opiates, produce analgesia. Such modulation of pain occurs through connections of this analgesia center with neurons of the nucleus raphe magnus and adjacent reticular formation at the pontomedullary junction. Axons descend from these
nuclei to the region of the substantia gelatinosa and secondary spinal pain neurons where the transmission of ascending pain impulses is inhibited.
What are the diffuse modulating systems? Where are they located generally? What are 3 major features of them?
Diffuse Modulating Systems
Several groups of neurons in the brainstem reticular formation form the diffuse modulating systems. Each of these groups is associated with a particular neurotransmitter which is widely dispersed in various parts of the CNS. Functionally, these systems regulate the excitability of vast numbers of neurons, making them more or less excitable.
There are three major features of these systems:
1) each has a relatively small number of neurons, i.e., 10,000 to 15,000; 2) the axon of each neuron travels a great distance, has innumerable branches, and may influence more than 100,000 widely spread postsynaptic neurons; 3) the neurotransmitters are released into the
extracellular fluid where it can diffuse to many neurons.
What nucleus is involved in the noradrenergic modulating system? What is it located? Where is its output? What funcitons is it involved in? What does it increase?
- noradrenergic locus ceruleus
a) located in the lateral part of the floor of the rostral pontine fourth ventricle
b) axons distributed to entire cerebral cortex, thalamus, hypothalamus, cerebellum, midbrain, and spinal cord
c) involved in regulation of attention, cortical arousal, sleep-wake cycle, as well as learning, memory, anxiety, mood
d) increases brain responsiveness, speeding information processing
Which nuclei are involved in the serotonergic modulating system? Where are they located? What is their output? What functions are they involved in?
- serotonergic raphe nuclei
a) neurons clustered in raphe nuclei
b) medullary project to spinal cord for modulation of slow pain
c) pontine and midbrain project to the thalamus, limbic nuclei, and cerebral cortex
d) involved in sleep/wake cycle; also implicated in control of mood and certain types of emotional behavior, especially aggression
What nuclei are involved int he dopaminergic system? Where do they project? What functions are they involved with?
- dopaminergic substantia nigra (SN) and ventral tegmental area (VTA)
a) SN projects to striatum
b) VTA projects to prefrontal cortex and limbic nuclei
c) VTA associated with reward and pleasure
What nuclei are involved int he cholinergic system? Where are they located? Where do the pontine and midbrain nuclei project? Where do the forebrain nuclei project? What does each regulate? What is degeneration of basal nucleus associated with?
- cholinergic brainstem and basal forebrain system
a) pontine and midbrain nuclei project to thalamus - regulate excitability of sensory relay nuclei
b) basal forebrain nuclei (basal nucleus of Meynert) project to cerebral cortex - regulate cortical excitability, memory, and learning
c) degeneration of basal nucleus associated with loss of cognitive functioning; occurs in Alzheimer’s disease
Where is the respiratory center located in the RF? How does it regulate respiration? What kind of damage leads to respiratory arrest? What kind of input does the respiratory center receive?
Respiration – The respiratory center is located bilaterally in the ventrolateral medullary reticular formation at the caudal part of the fourth ventricle. During inspiration it sends reticulospinal fibers to the phrenic nucleus at C.3 and 4 and to other lower motor neurons at T.1 to T.10 that innervate the intercostal muscles. Bilateral lesions of the respiratory center or its descending projections results in respiratory arrest.
The respiratory center receives input from the carotid and aortic bodies via the IX and X nerves respectively, as well as from various centers in the brainstem (pneumotaxic and apneustic) and forebrain, which will be described later.
How is the brainstem involved in REM and NREM sleep? Which parts? What lesion will result in insomnia?
Sleep – Sleep is characterized by two stages: rapid eye movement (REM) and non-rapid eye movement (NREM). REM sleep is generated by groups of neurons in the pons, while NREM sleep is generated by groups of neurons in the hypothalamus and all parts of the brainstem. The actual circuitry regulating sleep is extremely complex and poorly understood. However, it seems clear that the anterior hypothalamus induces sleep since lesions here
result in insomnia.
What part of the RF is involved in waking the cerebral cortex? What happens if its damaged? How does impairment of this system usually occur? What happens if the damage is irreversible?
Cerebral cortex - ascending through the reticular formation is a system of impulses that pace cortical activity. These impulses are collectively referred to as the “Ascending Reticular Activating System” (ARAS). The importance of this system is dramatized by experimental studies which have shown that even with intact sensory pathways, the cerebral cortex cannot be aroused from a comatose state if there is interruption of ARAS by bilateral
lesions in the paramedian midbrain reticular formation. This ascending system is able to activate or inactivate the cortex and is responsible for the various degrees of consciousness.
Impairment of this system frequently occurs in herniation (uncal) wherein the midbrain shifts or twists interrupting the ARAS and resulting in coma. If the damage is irreparable the coma is irreversible.
