This semester, we will focus our attention on the structures and functions of the central nervous system and how they support or interfere with occupational performance and participation. In this section, topics that we will explore include:
the neurodevelopment and maturation of basic structures of the central nervous system.
its gross structures and functions
neuroreceptors and neurotransmitters
the arterial supply of the central nervous system
cranial nerves
A deep exploration of these topics sets a solid groundwork for topics that follow: common neurological conditions seen in occupational therapy practice, including cerebral palsy, autism spectrum disorder, pain perception, vision and visual perception, hearing and balance, cerebrovascular accidents, major depressive disorder, alcohol use disorder, and mild cognitive impairment and Alzheimer’s dementia. Students will also learn about the evaluation and interventions for these conditions in other courses throughout the curriculum.
LEARNING OBJECTIVES:
Describe the growth and differentiation of the neural tube.
Relate the different stages of development to the adult structures of the central nervous system.
Identify major structures of the central nervous system and their basic functions.
Describe the processes involved with neurotransmission over a chemical synapse.
Categorize major neurotransmitters by chemical type and their effect on the nervous system.
Identify major structures of the arterial supply of the central nervous system.
Given what you know about the functions of the various structures of the CNS, predict the deficits with which a client may present if one of the vessels is occluded. Which structures would be impacted? which functions would be impacted?
Describe the functions of the cranial nerves.
Conduct a cranial nerve screen.
Neurodevelopment: Maturation of the Central Nervous System
At the beginning of the third week after fertilization, embryonic cells differentiate into one of three germinal layers in a process called gastrulation.
Endoderm: The innermost layer that will give rise to the endocrine glands, gastrointestinal tract, and respiratory tract.
Mesoderm: The middle layer that will give rise to the musculoskeletal system, cardiopulmonary system, and other internal organs.
Ectoderm: The outermost layer that will give rise to the integumentary (skin) system and nervous system.
(Invitra, 2022)
Following gastrulation, rudimentary structures of the central nervous system begin to form from the ectoderm. This process of neural tube development is called neurulation.
The outer layer of the ectoderm thickens and forms what is known as the neural plate.
The sides of the neural plate begin to fold dorsally forming a groove known as the neural groove and the borders of the neural plate form the neural crest (sometimes referred to as the neural folds).
By the end of the fourth week, the neural crest has completely fused together and the neural groove forms what is known as the neural tube, which are the precursors for the brain and spinal cord.
(Betts et al., 2022, Fig. 28.13)
As the neural tube closes, the rostral portion begins to develop into the brain structures by forming three primary vesicles: the prosencephalon, mesencephalon, and rhombencephalon. See Figure (a) below. The caudal end of the neural tube will eventually develop into the spinal cord.
The prosencephalon will eventually develop into the forebrain.
The mesencephalon will eventually develop into the midbrain.
The rhombencephalon will eventually develop into the hindbrain.
The neural tube continues to develop and by the fifth week, the primary vesicles further differentiate into five secondary vesicles. See Figure (b) below. The prosencephalon differentiates into the telencephalon, which will eventually develop into the cerebrum and subcortical structures, and the diencephalon, which will eventually develop into the eye cup (precursor for the retina), thalamus, hypothalamus, and epithalamus. The mesencephalon does not further differentiate and will eventually form the most superior aspect of the brainstem. Finally, the rhombencephalon differentiates into the metencephalon, which will eventually develop into the pons and cerebellum, and the myelencephalon, which will eventually develop into the medulla oblongata. The pons and medulla form the more caudal part of the brainstem.
(Betts et al., 2022, Fig. 13.3)
Gross Structures and Functions of the Central Nervous System
Here, we’ll discuss the major structures of the central nervous systems (organized by the five secondary vesicles) and describe their primary functions. We’ll start with the more rostral structures and work our way caudally. Your understanding of these structures and their basic functions will be critical to understanding the clinical presentations of various pathology with which clients may present (Section 1.1.1 through Section 1.1.13). For each of the five secondary brain vesicles covered, complete the Activity for Critical Thinking (blue box) that will help you to review what has been presented.
Telencephalon > Cerebral cortex
As previously mentioned, the telencephalon develops into the cerebrum and subcortical structures. The cerebrum constitutes the largest structure by mass of the central nervous system. The cerebral cortex is the outer, wrinkled portion (grey matter) of the cerebrum and is densely packed with neurons that are associated with higher brain functions, such as executive functioning, motor planning and organization, language processing, vision, and memory. The bulges of the cerebral cortex are called gyri and the fissures are called sulci. Dividing the two hemispheres of the cerebrum is the longitudinal fissure. Deep within the longitudial fissure, the right and left cerebral hemispheres are joined by the corpus callosum, a major pathway for communication between the two hemispheres.
(Betts et al., 2022, Fig. 13.6)
You will recall that the cerebral cortex may be divided into four paired lobes: frontal lobes, parietal lobes, temporal lobes, and occipital lobes. The central sulcus divides the frontal lobes from the parietal lobes; the lateral sulcus divides the frontal and parietal lobes from the temporal lobe; and the parieto-occipital sulcus divides the parietal lobes from the occipital lobes. An interactive digital model of the four lobes of the cerebral cortex may be found by following this link
(Betts et al., 2022, Fig. 13.7)
Frontal lobe
The frontal lobes are the largest lobes of the cerebral cortex. They are located rostrally in the cranial vault. The frontal lobes themselves can be subdivided into different functional areas. Here, we’ll cover five areas that are most relevant to clinical practice: prefrontal cortex, primary motor cortex, medial and lateral premotor cortices, and Broca’s area.
The prefrontal cortex, which is located along the dorsolateral frontal lobe, manages and coordinates executive functioning (e.g., decision-making, problem-solving, empathy, insight, flexibility, emotional regulation, morality, and intuition). Lesions in this area result in a number of neuropsychiatric disorders that present with disinhibition, apathy, loss of initiative, and personality changes (Hathaway & Newton, 2023).
The primary motor cortex and supplemental motor area lie anterior to the central sulcus in the precentral gyrus and organize motor behavior. Collectively, they are responsible for programming, planning, and voluntary control of motor responses. You may want to review the sensorimotor feedback loop discussed in Section 8.2.
(Augustine et al., 2024, Fig. 17.2)
The primary motor cortex (M1) is the source of most of the upper motor neurons that extend to the corticospinal (between the cortex and spinal cord) and corticobulbar (between the cortex and brainstem) tracts. Sections of the primary motor cortex may be stimulated to produce movement of specific body parts, depending on the area stimulated. The image to the right describes a homunculus that maps the specific areas of the primary motor cortex to different parts of the body.
(Knierim, 2020a, Fig. 3.3)
Representations of body parts that perform more precise, delicate movements (such as the hands and face) are disproportionately large on the homunculus in comparison to body parts that perform more coarse, unrefined movements (such as the trunk or legs). A lesion in the primary motor cortex will result in contralateral hemiparesis, which we’ll explore in greater detail in Section 8.1.5 (cerebrovascular accidents, or stroke).
The primary motor cortex also encodes the force, direction, distance, and speed of movement (Knierim, 2020a). A person with damage to the primary motor cortex may also present with dyscoordination (e.g., over- or under-shooting a target when reaching, applying too much or too little force in grip, etc.).
The supplementary motor area (SMA), sometimes called the supplementary motor cortex or secondary motor cortex (M2), lies anterior to the primary motor cortex (M1). It can be divided into two regions: the medial premotor cortex and the lateral premotor cortex.
The medial premotor cortex is located in the superomedial position and is primarily responsible for initiation of movement, orientation of the eyes and head, and planning bimanual and sequential movements (Lundy-Ekman, 2023). Lesions located in the medial premotor cortex result in apraxia. Apraxia may generally be described as the inability to perform coordinated movements, despite sensation, strength, and muscle tone being normal. A person with apraxia may understand the task to be performed and can verbally describe the sequence of actions to be performed, but cannot effectively demonstrate the task.
The lateral premotor cortex is located inferolateral to the medial premotor cortex. The lateral premotor cortex is primarily responsible for the organization and planning of motor actions, especially those that require visual or somatosensory input. For example, a motor plan for reaching for a mug of coffee. Additionally, it is also responsible for stabilization of the shoulder and pelvic girdles and making postural adjustments of the trunk during reaching and walking activities (Lundy-Ekman, 2023).
Broca’s area is the region of the frontal lobe of the dominant hemisphere (usually the left) that is responsible for the motor commands involved in speech production. More specifically, Broca’s area is important for assigning meaning to words (semantics), how words should sound (phonology), gesture production, sentence grammar and fluidity, and the interpretation of others’ actions (Stinnett et al., 2023). It is located in the inferior frontal gyrus, inferolateral to the lateral premotor cortex and anterior to the primary motor cortex. Lesions in Broca’s area result in expressive (or non-fluent) aphasia, where the client is unable to speak in a coherent manner. Words are lost or substituted and sometimes grammar is compromised (Acharya & Wrten, 2023). To view a short video that explains two different kinds of aphasia, follow this link. To view a short video of a person with Broca’s aphasia, follow this link.
(Khatouri, 2021, Fig. 2)
Parietal lobe
The parietal lobes are located posterior to the frontal lobe and their margins include the central sulcus, parieto-occipital sulcus, and the lateral sulcus. There are two main functional areas of the parietal lobe on which we’ll focus here: the primary and secondary somatosensory cortices.
The primary somatosensory cortex (S1) is located in the postcentral gyrus, just posterior to the central sulcus at the most anterior portion of the parietal lobe. It receives peripheral sensory input from specific areas of the body. Just as there was a homunculus that describes motor connections to different areas of the body, there is a homunculus that maps sensory information. Lesions in the S1 cortex result in impairments in somatosensation such as paresthesia or hypoesthesia (e.g., numbness, tingling, or absence of sensation; inability to distinguish shape, size, and texture [Raju & Tadi, 2022]).
The secondary somatosensory cortex (S2) is located just inferolateral to the primary somatosensory cortex, just superior to the lateral sulcus (not pictured). The secondary somatosensory cortex receives input from the S1 cortex; it’s primary function is to process and integrate peripheral sensory information (Dougherty, 2020). Lesions in the S2 cortex are associated with impairments in spatial and tactile memory of sensory experiences (Raju & Tadi, 2022).
(Encyclopedia Brittanica, n.d.b)
Temporal lobe
The temporal lobes are located on either side of the cranial vault, from under the temple area of the skull to just behind the ears, posterior to the frontal lobes, inferior to the lateral fissure, and anterior to the occipital lobes. The primary functions of the temporal lobes include processing of visual and auditory input, learning and memory, emotional regulation, and speech perception and production (Patel et al., 2023).
(Patel et al., 2023, Figure 2)
Four functional areas of the temporal lobe on which we will focus include: Wernicke’s area, auditory cortex, fusiform gyrus, and the limbic system.
Wernicke’s area is the posterior region of the superior temporal gyrus of the temporal lobe of the dominant hemisphere (usually the left) that is responsible for speech comprehension (Javed et al., 2023). Lesions in Wernicke’s area result in receptive (or fluent) aphasia, where an individual’s ability to understand spoken or written words is compromised. As for speech production, individuals with Wernicke’s aphasia retain the prosody (rate, intonation, flow) of speech, but the meaning is lost due to substitution of words (Lui & Wroten, 2025). To view a short video of a person with Wernicke’s aphasia, follow this link.
(Encyclopedia Brittanica, n.d.a)
The auditory cortex is comprised of the primary auditory cortex (A1) and the secondary auditory cortex (A2) and is located in the superior temporal gyrus of the temporal lobe. The main function of the auditory cortex includes the processing of auditory stimulation. It is particularly adept at distinguishing sounds and speech (Augustine et al., 2024).
(Augustine et al., 2024, Fig. 10.13)
The fusiform gyrus is located along the inferior margin of the temporal lobe (not pictured). It is particularly important in facial recognition (Patel et al., 2023). Individuals with lesions of the fusiform gyrus experience prosopagnosia, or the inability to recognize the faces of familiar people (such as family members, partners, and friends).
The limbic system regulates lower order emotional processing, especially those emotions related to survival (e.g., anger, fear, joy, sadness, disgust, and surprise) and whose facial expressions are generally recognized across cultures (Simic et al., 2021). It also contributes to endocrine regulation, the functioning of the autonomic nervous system, and some aspects of cognition, specifically related to learning, memory, and motivation (Torrico & Abdijadid, 2023). while the limbic system involves cortical, subcortical, and diencephalic structures, we focus our attention on three of its main structures: the hippocampus, amygdala, and cingulate gyrus.
The hippocampus is a C-shaped portion of the cortex that folds into the medial temporal lobe’s surface. It plays a critical role in emotional processing, the conversion of short-term memory into long-term memory, and associative learning (Fogwe et al., 2023). Associative learning is the ability to understand the associations between behavior and consequences (or stimulus and response). Dysfunction of the hippocampus is often implicated in individuals with autism spectrum disorder (ASD), Alzheimer’s disease (AD), schizophrenia, and attention deficit hyperactivity disorder (ADHD).
The amygdala is an almond-shaped structure that is critical to emotional regulation, particularly for emotions such as fear and anxiety) and initiates the sympathetic nervous system (fight-flight response). It is involved in visual attention to faces (particularly the eye region) and in regulating the stimulation of appetite (AbuHasan et al., 2023). It is implicated in individuals with post-traumatic stress disorder (PTSD), autism spectrum disorder (ASD), Alzheimer’s disease (AD), anxiety disorders (including panic disorder), major depressive disorder (MDD), and substance use disorder (SUD, or addiction).
The cingulate cortex wraps itself around the superior aspect of the corpus callosum. It contributes to processing and regulating emotions, reward-based decision-making (motivation), and visual-spatial orientation (Jumah & Dossani, 2023). Lesions in the cingulate gyrus result in flat affect (absence of emotions), lack of empathy, impaired attention, and loss of cognitive flexibility. Abnormal cingulate gyri have been observed in people with schizophrenia (Jumah & Dossani, 2023; Yucel et al., 2003), obsessive-compulsive disorder (OCD), depressive disorders, post-traumatic stress disorder (PTSD), and autism spectrum disorder (ASD; Yucel et al., 2003).
(Betts et al., 2022, Fig. 15.12)
Occipital lobe
The occipital lobes are located at the posterior of the cranial vault, posterior to the parietal and temporal lobes and superior to the cerebellum. They are the smallest of the four lobes of the cerebral cortex. The occipital lobes’ main function is the processing of visual information from the retinas. The two main functional areas of the occipital lobes that we’ll discuss are the primary visual cortex and secondary visual cortex.
The primary visual cortex (V1) is the first part of the occipital lobe that receives information from the retinas in the eyes via the lateral geniculate nuclei in the thalamus in the diencephalon. The visual cortices of each hemisphere receives input from the contralateral visual field. In other words, the right visual cortex receives input from the left visual field and vice versa. Lesions of V1 result in cortical vision impairment.
The secondary visual cortex (V2) surrounds and receives input from V1, where it analyzes visual input in terms of differentiation of color, pattern complexity, object orientation, and object recognition (Huff et al., 2023).
We will explore the visual pathways and pathologies in the visual system in greater detail in Section 8.1.4.
(Encyclopedia Brittanica, n.d.a)(Sheffield, 2022)
Telencephalon > Subcortical nuclei
Deep in the cerebrum lie the subcortical structures collectively known as the basal ganglia, which develops from the telencephalon. The basal ganglia are a clustering of nerve cell bodies that augment cortical processes. You will note in many texts, the basal ganglia are comprised of three parts: corpus striatum, substantia nigra, and subthalamic nucleus. It is beyond the scope of this Course Manual to explain the specific functions of each of these structures, but will be mentioned here only in passing. The corpus striatum is comprised of the caudate nucleus and the lentiform nucleus (which itself is comprised of the putamen and globus pallidus internus and externus). For a visualization of the structures and substructures, please see the figures below.
(modified from Andrusca, 2023)Components of the basal ganglia
As depicted in the illustration above, the various structures of the basal ganglia arise from the telencephalon, diencephalon, and mesencephalon. Here, we’ll keep our focus on the basal ganglia more globally, as a set of structures, rather than each individual structure. While the basal ganglia are associated with reward seeking behavior, learning, emotional regulation, and habit formation, its primary function is in regulating voluntary motor control, specifically assisting with the initiation of motor movement (Young et al., 2023).
Motor functions: As you recall, voluntary movement is initiated in the supplementary motor area (SMA) and executed by the primary motor cortex (M1) in the frontal lobe. The basal ganglia are involved in the selection of appropriate movement patterns from the library of motor plans stored in memory and the inhibition of competing motor plans (Knierim, 2020b). For example, in bringing one’s hand to the face for feeding, the basal ganglia assist the SMA and M1 with selecting the complex motor plan to do that, including timing the initiation of the movement; speed, force, and accuracy of movement required; and making sure that the motor plan for holding one’s hand to the face when protecting it from a thrown object is not selected. The basal ganglia are also implicated when developing a new motor plan, such as when first learning to ride a bicycle. Lesions of the basal ganglia result in movement disorders (dyskinesias) such as Parkinson’s disease, Tourette’s syndrome, and Huntington’s disease, where involuntary movements, tremors, or tics are present. To view a brief video demonstrating a few people with motor disorders of the basal ganglia, follow this link.
Cognitive/affective functions: The basal ganglia collectively also have connections with the prefrontal cortex in the frontal lobe and the limbic system in the temporal lobe. Just as was the case with motor functions, the basal ganglia are involved in the selection of cognitive, executive, and emotional programs that are stored in these other cortical areas (Knierim, 2020b). In particular, the basal ganglia are involved in associative learning (stimulus-response), motivation-reward, and habit formation. Lesions in the basal ganglia are also associated with eating disorders, obsessive-compulsive disorders, depressive disorders, anxiety disorders, substance use disorders, attention deficit hyperactivity disorder, and schizophrenia (Macpherson & Hikida, 2019).
(Betts et al., 2022, Fig. 13.9)
ACTIVITY FOR CRITICAL THINKING #1:
Thus far, we’ve discussed the many structures that arise from the telencephalon. These include the four lobes of the cerebral cortex and the basal ganglia. To help you better organize this information in a meaningful way, download this document with a table of the structures and try filling in the right-hand column of function and dysfunction. Start with the structures of the telencephalon; we’ll get to the other secondary brain vesicles later. As mentioned at the beginning of this Section (8.1), Sections 1.1.1 through 1.1.13 will examine clinical conditions that result due to pathology.
The second secondary vesicle is the diencephalon, which arises from the prosencephalon (forebrain). It is a clustering of neural tissue that lies between the cerebrum and brain stem and mainly serves as the relay and processing center for sensory and motor information between the telencephalon and the mesencephalon, metencephalon, and myelencephalon. It should be noted that the subthalamic nucleus and substantia nigra (parts of the basal ganglia) arise from the diencephalon and mesencephalon, respectively, but are identified here because they are part of the basal ganglia. The diencephalon also controls the autonomic nervous system (which regulates involuntary body processes, such as heart rate, respiration rate, and blood pressure). Here, we’ll focus our discussion on four main structures of the diencephalon that we have not yet discussed: thalamus, hypothalamus, epithalamus, and pituitary gland.
The thalamus consists of two oval nuclei that sit on either side of the diencephalon (pictured in green below) and constitute the majority of the mass of the diencephalon. Its primary function is to act as a primary relay station between the basal ganglia and the cerebral cortices. All sensory information from the peripheral nervous system (with the exception of olfaction [sense of smell]) synapses within the thalamus before travelling to the sensory cortices in the parietal lobes, the auditory cortices in the temporal lobes, or the visual cortices in the occipital lobes. Likewise, it is the relay station for signals from the motor cortices in the frontal lobes to the cerebellum and spinal cord for executing movement, thus completing the sensorimotor feedback loop discussed in Section 8.2 of the Course Manual. Additionally, the thalamus plays a role in the regulation of the sleep-wake cycle, arousal states (levels of alertness), modulation of pain and temperature, motor aspects of language production, some cognitive functions (including executive functions, attention, learning, and memory), mood regulation, and motivation (Torrico & Munakomi, 2023). Dysfunction of the thalamus is associated with memory loss (amnesia), lack of interest or motivation (anhedonia), expressive and receptive aphasia, sleep disorders, changes in arousal states (e.g., coma), pain disorders, movement disorders, and visual disorders (Cleveland Clinic, n.d.).
The hypothalamus is a small structure of the inferior diencephalon that sits at the top of the brainstem (pictured in orange below). Its primary functions are to regulate two functions: metabolic functions of the body and the autonomic nervous system (Shahid et al., 2023), including maintaining homeostasis through endocrine regulation (e.g., mood, growth and development, organ function, reproduction), body temperature, circadian rhythm (sleep-wake cycle), inflammatory response (e.g., corticosteroids), and food intake (hunger-satiety).
The epithalamus is located at the posterior portion of the diencephalon (pictured in blue below). It mostly functions to connect the limbic system with the rest of the body and contributes to emotional regulation. One of the major structures of the epithalamus is the pineal gland, which regulates the sleep-wake cycle through the secretion of melatonin.
The pituitary gland is a small structure at the base of the hypothalamus that secretes hormones that regulate growth and development, organ function (e.g., metabolism, reproduction), and physiological response to stress or trauma.
(Betts et al., 2022, Fig. 13.11)
ACTIVITY FOR CRITICAL THINKING #2:
As you did with the telencephalon, complete the right-hand column of the table, filling in the functional aspects of the named structures.
Mesencephalon
The mesencephalon (midbrain) is the third secondary vesicle of the brain; it is located between the diencephalon and rhombencephalon at the superior aspect of the brainstem and functions to connect the two. There are three primary structures of the mesencephalon on which we will focus: tectum, tegmentum, and cerebral peduncles.
The tectum is located at the dorsal aspect of the midbrain and is comprised of two rounded masses, the superior and inferior colliculi (singular = colliculus). The superior colliculus has connections with the retina in the eye and the visual cortex in the occipital lobe and processes visual information, including coordinating eye movements while tracking an object in the visual field. We will explore the visual system in greater depth in Section 8.1.4. The inferior colliculus has connections with the auditory cortex in the temporal lobe and processes and integrates auditory information.
The tegmentum is located in the rostral portion of the mesencephalon and is divided into several distinct areas, each with specific functions. The red nucleus and the substantia nigra both contribute to motor coordination, particularly with locomotion (e.g., crawling in quadruped and gait) and bimanual activities. Lesions in these areas results in dyscoordination (e.g., tremors and ataxia, such as that demonstrated in Parkinson’s disease). Parts of the reticular activating system (RAS), which is responsible for the regulation of arousal states, are also located within the tegmentum. The RAS contributes to arousal states, attention, and motivation. Dysfunction of the RAS is associated with conditions such as schizophrenia, PTSD, sleep disorders, Parkinson’s disease, and attention deficit hyperactivity disorder (Arguinchona & Tadi, 2023).
The cerebral peduncles lie on each side of the brainstem, along the anterior surface inferior to the tectum. Its primary function include relaying sensory information from the cerebral cortices and thalamus to the spinal cord and refining motor coordination required for balance and postural control.
(Arguinchona & Tadi, 2023)
ACTIVITY FOR CRITICAL THINKING #3:
As you did with the previous parts of the brain structures, complete the right-hand column of the table, filling in the functional aspects of the named structures.
Rhombencephalon > Metencephalon
The fourth secondary vesicle of the brain is the metencephalon. The metencephalon arises from the rhombencephalon (hindbrain) and is located between the mesencephalon and myelencephalon, at the caudal end of the brainstem. There are two structures on which we will focus our attention: the pons and cerebellum.
The pons is the more rostral part of the metencephalon and is located ventral to the cerebellum. The main function of the pons is to transmit signals between the cerebral cortices and the cerebellum and spinal cord. It contributes to the regulation of breathing functions, sleep-wake cycle, equilibrium and balance, facial expression, oculomotor function, mastication (chewing), and pain sensation (Rahman & Tadi, 2023). Injury to the pons may result in decreased arousal, dysequilibrium (loss of balance), diplopia (double vision), dysphagia (difficulty swallowing), and slurred speech.
The cerebellum is the largest structure of the metencephalon, located dorsal to the pons and caudal to the occipital lobe. The cerebellum is grossly divided into two hemispheres and a vermis (which lies along the medial divide between the hemispheres). It receives sensory information about voluntary muscle movements from the sensory cortex in the parietal lobes and vestibular input from the temporal lobes. The cerebellum’s function is to regulate and refine balance and posture, muscle tone, motor control, language processing, emotional regulation, oculomotor function for visual-spatial relations, and executive functioning (Jimshileishvili & Dididze, 2023). Dysfunction of the cerebellum may result in dysdiadochokinesia (difficulty performing rapid alternating movements), ataxia, nystagmus (rapid, uncontrolled eye gaze), intention tremors, or slurred speech (Ataullah et al., 2024).
(Moawad, 2024)(TeachMe Anatomy, n.d., Fig. 1)
ACTIVITY FOR CRITICAL THINKING #4:
As you did with the previous parts of the brain structures, complete the right-hand column of the table, filling in the functional aspects of the named structures.
Rhombencephalon > Myelencephalon
The final (fifth) secondary vesicle of the brain is the myelencephalon. It arises from the most caudal portion of the rhombencephalon (hindbrain) just rostral to the spinal cord. The myelencephalon is composed of the medulla oblongata, which is responsible for cardiovascular and pulmonary functioning (Iordanova & Reddivari, 2023) and is part of the reticular activating system discussed in the section on the mesencephalon. Ascending sensory and descending motor corticospinal tracts cross midline from the spinal cord to the thalamus here in a process called “decussation”. Additionally, the nuclei of four of the twelve cranial nerve lie within the medulla. As a result, the medulla controls the reflexes of the digestive tract (including cough, gag, and swallow reflexes).
(OpenStax, 2016, Fig. 13.12)
DIGITAL ANATOMY REVIEW:
Follow these links to 4D Interactive Anatomy (PNWU OT – Gross Structures of the CNS) to view digital scans of the central nervous system. Note: You must be logged in to the site before clicking the link).
As you did with the previous parts of the brain structures, complete the right-hand column of the table, filling in the functional aspects of the named structures.
Neurons in the central nervous system communicate with each other through one of two means: an electrical synapse and a chemical synapse (Purves et al., 2004). Of the approximately 86 billion neurons (Caire et al., 2023) in the brain, chemical synapses far outnumber electrical synapses.
(Purves et al., 2004, Fig. 5.1)
In an electrical synapse (also known as a gap junction), there is a physical, mechanical link between two neurons. The presynaptic and post-synaptic membranes are touching and the gap junction channels permit the flow of ions across the membranes to propagate the action potential.
In a chemical synapse, there is a physical space called a synaptic cleft (also known as a synaptic gap) between the presynaptic membrane and post-synaptic membrane. The synaptic cleft measures between 10 and 20 nanometers (Vanderah & Gould, 2022). One nanometer (10-9 meters) is one billionth of a meter. There are six steps for action propagation in chemical synapses:
The presynaptic element is the neuron located before the synaptic cleft. It is the one propagating the action potential (i.e., the “sender” neuron). The action potential of the presynaptic element reaches the axon bulb.
Calcium ions (Ca2+) accumulate in the terminal bulb of the presynaptic element.
Neurotransmitters are packaged in the presynaptic elements in synaptic vesicles. The calcium ions associate with the membrane of the synaptic vesicles and facilitate the movement of the vesicles toward the synaptic membrane.
The neurotransmitters are released into and travel across the synaptic cleft.
Neurotransmitter-specific post-synaptic receptors absorb the neurotransmitters. In other words, receptors only absorb a specific kind of neurotransmitter and repel other kinds of neurotransmitters.
The neurotransmitters are absorbed into the post-synaptic membrane and propagate the action potential in the post-synaptic element.
Chemical synapse (Betts et al., 2022, Fig. 12.27)
While there are over 100 different types of neurotransmitters (Caire et al., 2023), we will focus our attention on seven, which fall into one of two categories based on their effect on target neurons: excitatory or inhibitory. There are also a few neurotransmitters that are both excitatory and inhibitory; these we will call modulatory neurotransmitters.
Excitatory neurotransmitters have a stimulatory effect by propagating the action potential of post-synaptic neurons (Sheffler et al., 2023).
Epinephrine (also known as adrenaline) is both a hormone and a neurotransmitter. As a hormone, epinephrine is produced by the adrenal glands, which are located just superior to the kidneys, in response to stressors or perceived threats. It plays a role in the regulation of the sympathetic nervous system in a “fight-or-flight” response and results in increased heart rate and blood pressure, pupillary dilation, and decreased sensitivity to pain. High levels of epinephrine are implicated in people with hypertension, panic disorders, anxiety disorders, the manic phases of bipolar disorders, aggression, agitation, and psychosis. Low levels of epinephrine are implicated in depressive disorders, fatigue, difficulties with memory, and low motivation.
Like epinephrine, norepinephrine (also known as noradrenaline) is also a hormone and neurotransmitter. It is produced in the brainstem in an area that is part of the reticular activating system (RAS) and is released during periods of stress in the “fight-or-flight” response. Norepinephrine is molecularly different from epinephrine (and thus has different post-synaptic receptors), but it’s effects on the body systems are the same. It has a role in modulating arousal levels, attention, and the feeding cycle. High levels of norepinephrine are implicated in people with hypertension, panic disorders, anxiety disorders, the manic phases of bipolar disorders, aggression, agitation, and psychosis. Low levels of norepinephrine are implicated in depressive disorders, fatigue, difficulties with memory, and low motivation.
Glutamate may be considered the principal excitatory neurotransmitter in the CNS because of its abundance (Stallard et al., 2022). Its primary function is to tell other neurons to release their neurotransmitters and has been called the “master neurotransmitter” (Pal, 2021). It has a role in regulating short-term memory, encoding short-term to long-term memory, and associative memory. Additionally, glutamate is important in the regulation of mood (Pal, 2021). Excessive levels of glutamate are implicated in schizophrenia, anxiety disorders, autism spectrum disorders, Alzheimer’s dementia, bipolar disorder, Amyotrophic Lateral Sclerosis (ALS), and chronic pain (Stallard et al., 2022). Low levels of glutamate are implicated in antisocial behavior, hyperactivity, aggression, and depressive disorders (Pal, 2021).
While acetylcholine (ACh) works on many different parts of the body as an excitatory neurotransmitter, it is most commonly associated with the stimulation of muscle tissue at the neuromuscular junction. A neuromuscular junction is where the motor neuron synapses with muscle fibers to stimulate its contraction. When a motor neuron is stimulated, the action potential travels down the axon to the synaptic end bulb at the distal end. Vesicles located in the end bulb of the presynaptic motor neuron contain ACh, which are released into the synaptic cleft. ACh diffuses across the synaptic cleft and binds to ACh receptors on the motor end plate of the post-synaptic muscle fiber. When ACh binds to the receptors, sodium channels in the motor end plate open, allowing for the influx of sodium ions to flow. This activates the action potential in the motor end plate, causing myofibril contraction (see Section 7.2 for a review of muscle fibers and sarcomeres).
(Betts et al., 2022, Fig. 10.6)
ACh is also produced in the terminal ends of neurons in the basal ganglia and tegmentum of the mesencephalon (Sam & Bordoni, 2023). Besides stimulating muscle tissue, ACh affects the M1 receptors in the primary motor cortex of the frontal lobe and in the hippocampus (Sam & Bordoni, 2023). Low levels of ACh can cause deficits in learning and memory, particularly with retrieval of old motor plans and establishing new motor plans. Low levels are implicated in Alzheimer’s dementia (Sam & Bordoni, 2023); autism spectrum disorder, schizophrenia, and attention deficit hyperactivity disorder (Mental Health American [MHA], n.d.). Elevated levels of ACh are associated with depressive disorders (MHA, n.d.).
Inhibitory neurotransmitters have an inhibitory effect by reducing the likelihood of propagation of an action potential of post-synaptic neurons.
Gamma-aminobutyric acid (GABA) is considered to be the primary inhibitory neurotransmitter in the CNS. It is synthesized in the presynaptic end bulb and stored in the vesicles. When GABA is released into the synaptic cleft, it binds with GABA receptors in the post-synaptic membrane and inhibits the production of an action potential in the post-synaptic neuron (Jewett & Sharma, 2023). Many pharmacologic agents (medications) are used to bind to the GABA receptors, thus mimicking GABA’s inhibition of action potentials. Some examples include sedatives (Jewett & Sharma, 2023) used in anesthesia (e.g., propofol), barbiturates for seizure management (carbamazapine, benzodiadepine), withdrawal symptoms associated with alcohol use disorder and opioid dependence (e.g., naltrexone), muscle relaxants (e.g., baclofen), and analgesics used for neuropathic pain (e.g., gabapentin). High levels of GABA often result in drowsiness during the day, lethargy, difficulty concentrating, and cloudy thinking. Low levels of GABA are implicated in mood disorders (such as depressive disorders and anxiety disorders), schizophrenia, autism spectrum disorder, and attention deficit hyperactivity disorder.
Modulatory neurotransmitters work in conjunction with other neurotransmitters, enhancing the excitatory or inhibitory responses of receptors; they “tweak” or enhance how neurons communicate at the synaptic cleft. They have no direct effect on action potential propagation.
Serotonin is synthesized in the brainstem and the lining of the intestinal tract and regulates several body functions, including behavior, mood, memory, and gastrointestinal motility (Bamalan et al., 2023). Depending on the kind of chemical synapse, when serotonin enters the synaptic cleft, it either binds to presynaptic receptors (in a process called reuptake, which regulates the release of more serotonin into the synaptic cleft) or it binds to post-synaptic receptors (propagating the post-synaptic action potential). Excessive amounts of endogenous serotonin are implicated in the production of tremors, hyperreflexia, hypertonia, diaphoresis (excessive sweating in the absence of physical exertion), tachycardia, tachypnea, cardiac arrhythmia, agitation, confusion, and insomnia. Insufficient amounts of endogenous serotonin are implicated in major depressive disorder, post-traumatic stress disorder, obsessive-compulsive disorder, and anxiety disorder. A number of pharmacological agents (medications) in the treatment of psychiatric disorders target the body’s serotonin levels. Selective serotonin reuptake inhibitors (SSRIs) target pre-synaptic absorption of serotonin and are used in the treatment of anxiety and depressive disorders. Serotonin-norepinephrine reuptake inhibitors (SNRIs) also target pre-synaptic absorption of serotonin and are used in the treatment of anxiety, depression, and chronic pain. Monoaminoxidase inhibitors (MAOIs) target the enzyme monoaminoxidase, which degrades serotonin in the synaptic cleft. By inhibiting monoaminoxidase, MAOIs increase the amount of serotonin in the synaptic cleft to be absorbed by the post-synaptic neurons. Like SSRIs and SNRIs, MAOIs are used in the treatment of anxiety and depressive disorders.
Dopamine is synthesized in the substantia nigra (part of the basal ganglia) and plays a huge role in stimulus-response, motivation-reward behaviors, and habit formation (Sonne et al., 2023). While dopamine also acts as a hormone that increases cardiac conductivity, blood pressure, heart rate, and urine output, we focus our attention here primarily on dopamine as a neurotransmitter. Dopamine regulates motor learning and motor control. Elevated levels of endogenous dopamine are implicated in mania, schizophrenia, and substance use disorder. Insufficient levels of endogenous dopamine are implicated in autism spectrum disorder, depressive disorder, attention deficit hyperactivity disorder, and Parkinson’s disease.
Arterial Supply of the Central Nervous System
You’ll recall that in our discussion of the cardiovascular system (Section 10.1), the ascending aorta is the primary branch from the left ventricle of heart. It supplies freshly oxygenated blood to the rest of the body. The brachiocephalic artery is the first branch off the aortic arch and provides the blood supply to the right side of the body. From the brachiocephalic artery, the right common carotid artery supplies oxygenated blood to the right side of the head (including the brain). The left common carotid artery branches directly off the aortic arch and supplies oxygenated blood to the left side of the head and brain.
As the right and left common carotid arteries continue cranially, they branch into the internal and external carotid arteries. The external carotid arteries ascend toward the ear and provide blood supply to the neck and face. The internal carotid arteries supply oxygenated blood to the brain, eyes, extraocular muscles (the muscles that move the eye), upper nose, and parts of the forehead (Charlick & Das, 2023).
(Blausen, 2014)
You will also recall from our discussion of the vertebral column (Section 8.1) that the cervical vertebrae have transverse foramina located within the transverse processes. The transverse foramina protect the vertebral arteries on either side of the vertebral bodies.
(Betts et al., 2022, Fig. 20.24)
(Betts et al., 2022, Fig. 13.15)
We begin our discussion of the blood supply to the brain and brainstem with the internal carotid arteries and the vertebral arteries.
The internal carotid arteries supply about 80% of the blood supply to the brain, to most of the telencephalon. The internal carotid artery directly supplies oxygenated blood to the pituitary gland in the diencephalon. At the base of the brain, the internal carotid arteries bifurcate (divides into two) into the anterior cerebral artery and middle cerebral artery.
The anterior cerebral artery (ACA) passes anteriorly to supply blood to three lobes of the cerebral cortex and parts of the basal ganglia. In the frontal lobe, the ACA supplies oxygenated blood to the prefrontal cortex and the medial premotor cortex of the supplemental motor area (SMA). In the parietal lobe, the ACA supplies oxygenated blood to the primary somatosensory area (S1). In the temporal lobe, the ACA supplies oxygenated blood to the cingulate cortex of the limbic system. In the basal ganglia, the ACA supplies oxygenated blood to the corpus striatum (which includes the caudate nucleus, putamen, and globus pallidus internus and externus).
The middle cerebral artery (MCA) also supplies oxygenated blood to three lobes of the cerebral cortex and parts of the basal ganglia. In the frontal lobe, the MCA supplies oxygenated blood to the prefrontal cortex, the primary motor cortex (M1), the lateral premotor cortex, and Broca’s area. In the parietal lobe, the MCA supplies oxygenated blood to the primary somatosensory cortex (S1) and the secondary somatosensory cortex (S2). In the temporal lobe, the MCA supplies oxygenated blood to Wernicke’s area, the auditory cortex (A1, A2), and the amygdala in the limbic system. In the basal ganglia, the MCA supplies oxygenated blood to the corpus striatum (which includes the caudate nucleus, putamen, and globus pallidus internus and externus).
The vertebral arteries supply about 20% of the blood supply to the brain and brainstem, to most of the diencephalon and the mesencephalon.
When the vertebral arteries enter the cranial vault at the brainstem, they fuse to form the basilar artery. The basilar artery branches to form the cerebellar arteries and the pontine arteries, which supply oxygenated blood to the cerebellum and pons, respectively. As the basilar artery continues to the base of the brain, it bifurcates into the left and right posterior cerebral arteries (PCA). The PCA supplies oxygenated blood to two lobes of the telencephalon, most of the diencephalon, and parts of the mesencephalon. In the temporal lobe, the PCA supplies oxygenated blood to the fusiform gyrus and the hippocampus of the limbic system. In the occipital lobe, the PCA supplies oxygenated blood to the primary visual cortex (V1) and the secondary visual cortex (V2). In the diencephalon, the PCA supplies oxygenated blood to the subthalamic nucleus of the basal ganglia, the thalamus, and the epithalamus. In the mesencephalon, the PCA supplies oxygenated blood to the tegmentum, which is comprised of the red nucleus, substantia nigra of the basal ganglia, and parts of the reticular activating system. It also supplies oxygenated blood to the cerebral peduncles.
At the base of the rostral brainstem is the Circle of Willis, an apparent circle of arteries composed of the paired ACAs, MCAs, and PCAs (along with the anterior and posterior communicating arteries) in a process called “anastomosis” (a joining of two or more vessels, such as arteries).
Much of the mesencephalon and all of the metencephalon and myelencephalon are supplied by other arteries.
The basilar artery directly supplies oxygenated blood to thalamus.
The Circle of Willis directly supplies oxygenated blood to the hypothalamus.
The internal carotid arteries directly supply oxygenated blood to the pituitary gland.
The cerebellar arteries directly supply oxygenated blood to the superior and inferior colliculi of the tectum in the mesencephalon and the vermis and hemispheres of the cerebellum in the metencephalon.
The pontine arteries directly supply oxygenated blood to the pons in the metencephalon.
The vertebral arteries directly supply oxygenated blood to the medulla oblongata in the myelencephalon.
As an exercise to visualize the arterial blood supply to the central nervous system, download this schematic and cut (green dotted line), fold (purple dotted line), and tape (black dotted line) where indicated. The notations in blue indicate which structures are supplied with oxygenated blood.
Follow these links to 4D Interactive Anatomy (PNWU OT – Arterial supply of the CNS) to view digital scans. Note: You must be logged in to the site before clicking the link).
There are twelve cranial nerves that are primarily responsible for sensory and motor functions of the face and neck. They are designated CN-I through CN-XII, using “CN” for “cranial nerve” and Roman numerals to differentiate the twelve nerves.
CN-I: Olfactory nerve: a sensory nerve that is responsible for the sense of smell.
CN-II: Optic nerve: a sensory nerve that is responsible for vision. We will conduct a more in-depth exploration of the optic nerve’s role in the visual pathway in Section 8.1.4.
CN-III: Oculomotor nerve: a motor nerve that is responsible for moving the eye within the orbit. It is also responsible for raising the eyelids during superior gaze and for pupillary constriction in response to light. We will conduct a more in-depth exploration of the muscles of oculomotor function in Section 8.1.4.
CN-IV: Trochlear nerve: is a motor nerve that innervates one of the six extra-ocular nerves. We will conduct a more in-depth exploration of the muscles of oculomotor function in Section 8.1.4.
CN-V: Trigeminal nerve: has both sensory and motor components and is responsible for sensations of the face and for controlling the muscles of mastication (refer to Chapter 9).
CN-VI: Abducens nerve: is a motor nerve that innervates one of the six extra-ocular nerves. We will conduct a more in-depth exploration of the muscles of oculomotor function in Section 8.1.4.
CN-VII: Facial nerve: has both sensory and motor components and is responsible for detecting taste and for controlling the muscles for facial expressions. It is also responsible for salivary secretion.
CN-VIII: Vestibulocochlear nerve: previously called “Auditory nerve,” is a sensory nerve that is responsible for hearing and balance.
CN-IX: Glossopharyngeal nerve: has both sensory and motor components and is responsible for detecting taste and for controlling sensation and muscles of the oral cavity and oropharynx.
CN-X: Vagus: has both sensory and motor components and is responsible for parasympathetic control of visceral organs, affecting heart rate, breathing rate, and gastrointestinal motility. It also controls movement of the soft palate and uvula.
CN-XI: Accessory nerve: sometimes called “Spinal accessory nerve,” is a motor nerve that is responsible for control of laryngeal muscles, trapezius, and sternocleidomastoid.
CN-XII: Hypoglossal nerve: is a motor nerve that is responsible for controlling most of the muscles of the tongue.
Many students use mnemonic strategies to recall the cranial nerves in order, with a word being used to represent the first letter of each of the cranial nerves. “On Old Olympus’ Towering Tops, AFinn And German Viewed Some Hops.” However, cranial nerve naming conventions have changed, over time. Another mnemonic that reflects those changes is “Oh, Oh, Oh, To Touch And Feel Very Good Velvet AH!” Or perhaps you’ve heard of another. Students are encouraged to use whatever mnemonic works best.
(Betts et al., 2022, Fig. 13.23)
DIGITAL ANATOMY REVIEW:
Follow these links to 4D Interactive Anatomy (PNWU OT – Cranial nerves) to view digital scans of the cranial nerves. Note: You must be logged in to the site before clicking the link).
FOCUS ON CLINICAL APPLICATION:
Sometimes, occupational therapists are called upon to conduct a cranial nerve screening on a client as part of a comprehensive neurological exam. A cranial nerve screen identifies potential deficits of one or more cranial nerves. Conducting a cranial nerve screen may be administered in less than two minutes. Instructions are as follows (Taylor et al., 2021):
CN-I: Have the client close their eyes. Provide the client with a small vial that is scented (e.g., perfume, coffee, vanilla) and ask them to identify what’s inside (“Tell me what you smell.”). Note: Be sure that your client does not have chemical sensitivities.
CN-III: With the client seated in front of you, observe their eyelids and pupils for symmetry. Have the client focus on your nose while you use a penlight to shine a light on their pupils from the side. NEVER shine directly into the eyes. Observe for photopupillary response (pupils should constrict when exposed to the light). Test each eye separately.
CN-II, CN-III, CN-IV, & CN-VI: With the client sitting in front of you, hold out the penlight approximately two feet from the client. Ask them to follow the penlight as you move it in an “H”-pattern in the four visual quadrants. (“Follow the penlight as I move it around; try not to move your head.”)
CN-V & CN-VII: With the client sitting in front of you, have them clench their jaw as you palpate it. Have them smile, puff their cheeks, and raise their eyebrows. Observe for symmetry.
CN-VIII: With your client seated in front of you and with their eyes closed, place your thumb and index finger near each ear. Rub your thumb and index finger on one side, then the other. Have your client identify which side they hear the noise. (“I’m going to place my hands on either side of your head. I want you to tell me if you hear a noise on the right side or the left side.”). Alternatively, if the client is following your verbal directions thus far, it can be assumed that hearing is grossly intact.
CN-IX: With your client seated in front of you, instruct them to swallow their saliva. Observe for symmetry and difficulty.
CN-X: With your client seated in front of you, have the client open their mouth and say “Ahh.” Using a penlight, observe for soft palate and uvula elevation and symmetry.
CN-XII: With your client seated in front of you, have them stick out their tongue, then lateralize it side-to-side. Observe for strength and symmetry. NEVER stick your finger in their mouth. To test strength of lateralization, have them stick their tngue in their cheek, then press against their cheek with your finger.
CN-XI: With your client seated in front of you, have them shrug their shoulders. Press down firmly on each side with your hands. Observe for symmetry and strength.
A brief video of a cranial nerve screen being conducted may be viewed by following this link.
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