Anatomy of the Nervous System

The human nervous system can be divided into two interacting subsystems: the peripheral nervous system (PNS) and the central nervous system (CNS). The CNS consists of the brain and spinal cord. The peripheral nervous system is an extensive network of nerves connecting the CNS to the muscles and sensory structures. The relationship of these systems is illustrated below.

The Central Nervous System

The brain is the most complex and sensitive organ in the body. It is responsible for all functions of the body, including serving as the coordinating center for all sensations, mobility, emotions, and intellect. Protection for the brain is provided by the bones of the skull, which in turn are covered by the scalp, as shown below. The scalp is composed of an outer layer of skin, which is loosely attached to the aponeurosis, a flat, broad tendon layer that anchors the superficial layers of the skin. The periosteum, below the aponeurosis, firmly encases the bones of the skull and provides protection, nutrition to the bone, and the capacity for bone repair. Below the boney layer of the skull are three layers of membranes called meninges that surround the brain. The relative positions of these meninges are shown below. The meningeal layer closest to the bones of the skull is called the dura mater (literally meaning tough mother). Below the dura mater lies the arachnoid mater (literally spider-like mother). The innermost meningeal layer is a delicate membrane called the pia mater (literally tender mother). Unlike the other meningeal layers, the pia mater firmly adheres to the convoluted surface of the brain. Between the arachnoid mater and pia mater is the subarachnoid space. The subarachnoid space within this region is filled with cerebrospinal fluid (CSF). This watery fluid is produced by cells of the choroid plexus—areas in each ventricle of the brain that consist of cuboidal epithelial cells surrounding dense capillary beds. The CSF serves to deliver nutrients and remove waste from neural tissues.

Extended description

A wedge of scalp and skull is drawn cut away above a close-up circle of the brain’s surface. From outside in, the wedge labels skin, a thin aponeurosis layer, a thin periosteum layer, and bone. Inside the bone, a brace labeled Meninges spans three layers: the dura mater (drawn thickest, just under the bone), the arachnoid mater (a thinner layer below it), and the pia mater (a thin layer directly on the brain tissue). Between the arachnoid mater and the pia mater, the subarachnoid space is shown filled with cerebrospinal fluid (CSF) and containing blood vessels.

The Blood-Brain Barrier

The tissues of the CNS have extra protection in that they are not exposed to blood or the immune system in the same way as other tissues. The blood vessels that supply the brain with nutrients and other chemical substances lie on top of the pia mater. The capillaries associated with these blood vessels in the brain are less permeable than those in other locations in the body. The capillary endothelial cells form tight junctions that control the transfer of blood components to the brain. In addition, cranial capillaries have far fewer fenestra (pore-like structures that are sealed by a membrane) and pinocytotic vesicles than other capillaries. As a result, materials in the circulatory system have a very limited ability to interact with the CNS directly. This phenomenon is referred to as the blood-brain barrier.

The blood-brain barrier protects the cerebrospinal fluid from contamination, and can be quite effective at excluding potential microbial pathogens. As a consequence of these defenses, there is no normal microbiota in the cerebrospinal fluid. The blood-brain barrier also inhibits the movement of many drugs into the brain, particularly compounds that are not lipid soluble. This has profound ramifications for treatments involving infections of the CNS, because it is difficult for drugs to cross the blood-brain barrier to interact with pathogens that cause infections.

The spinal cord also has protective structures similar to those surrounding the brain. Within the bones of the vertebrae are meninges of dura mater (sometimes called the dural sheath), arachnoid mater, pia mater, and a blood-spinal cord barrier that controls the transfer of blood components from blood vessels associated with the spinal cord.

To cause an infection in the CNS, pathogens must successfully breach the blood-brain barrier or blood-spinal cord barrier. Various pathogens employ different virulence factors and mechanisms to achieve this, but they can generally be grouped into four categories: intercellular (also called paracellular), transcellular, leukocyte facilitated, and nonhematogenous. Intercellular entry involves the use of microbial virulence factors, toxins, or inflammation-mediated processes to pass between the cells of the blood-brain barrier. In transcellular entry, the pathogen passes through the cells of the blood-brain barrier using virulence factors that allow it to adhere to and trigger uptake by vacuole- or receptor-mediated mechanisms. Leukocyte-facilitated entry is a Trojan-horse mechanism that occurs when a pathogen infects peripheral blood leukocytes to directly enter the CNS. Nonhematogenous entry allows pathogens to enter the brain without encountering the blood-brain barrier; it occurs when pathogens travel along either the olfactory or trigeminal cranial nerves that lead directly into the CNS. For example, Naegleria fowleri, the “brain-eating amoeba,” reaches the brain after entering the body through the nasal canal and attaching to the olfactory nerve.

Most medicines, such as antiretroviral therapies (ART) and anti-cancer drugs, cannot penetrate the blood-brain barrier to treat illness or eradicate pathogens. The brain thus becomes a reservoir for infections. For example, HIV eradicated elsewhere in the body can survive the brain, where it can lead to cognitive decline and also can reseed the infection more widely. Researchers such as Johns Hopkins’ Dionna Williams study the impact of these persistent infections as well as the mechanisms that enable the pathogens to cross the barrier. She has identified the specific proteins that allow HIV-infected monocytes to cross, and notes the role that dopamine plays in barrier permeability. Williams also researches the mechanisms and impact of cocaine and opioids on the blood-brain barrier, which could lead to treatments for problematic substance use and potentially utilizing the drugs’ barrier-migration mechanisms. Williams and her team have also developed an antibody capable of crossing the barrier to kill HIV-infected cells. The promise of this work goes far beyond HIV, because these methods could be applied to the wide array of diseases for which the blood-brain barrier inhibits treatment.

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The Peripheral Nervous System

The PNS is formed of the nerves that connect organs, limbs, and other anatomic structures of the body to the brain and spinal cord. Unlike the brain and spinal cord, the PNS is not protected by bone, meninges, or a blood barrier, and, as a consequence, the nerves of the PNS are much more susceptible to injury and infection. Microbial damage to peripheral nerves can lead to tingling or numbness known as neuropathy. These symptoms can also be produced by trauma and noninfectious causes such as drugs or chronic diseases like diabetes.

The Cells of the Nervous System

Tissues of the PNS and CNS are formed of cells called glial cells (neuroglial cells) and neurons (nerve cells). Glial cells assist in the organization of neurons, provide a scaffold for some aspects of neuronal function, and aid in recovery from neural injury.

Neurons are specialized cells found throughout the nervous system that transmit signals through the nervous system using electrochemical processes. The basic structure of a neuron is shown below. The cell body (or soma) is the metabolic center of the neuron and contains the nucleus and most of the cell’s organelles. The many finely branched extensions from the soma are called dendrites. The soma also produces an elongated extension, called the axon, which is responsible for the transmission of electrochemical signals through elaborate ion transport processes. Axons of some types of neurons can extend up to one meter in length in the human body. To facilitate electrochemical signal transmission, some neurons have a myelin sheath surrounding the axon. Myelin, formed from the cell membranes of glial cells like the Schwann cells in the PNS and oligodendrocytes in the CNS, surrounds and insulates the axon, significantly increasing the speed of electrochemical signal transmission along the axon. The end of an axon forms numerous branches that end in bulbs called synaptic terminals. Neurons form junctions with other cells, such as another neuron, with which they exchange signals. The junctions, which are actually gaps between neurons, are referred to as synapses. At each synapse, there is a presynaptic neuron and a postsynaptic neuron (or other cell). The synaptic terminals of the axon of the presynaptic terminal form the synapse with the dendrites, soma, or sometimes the axon of the postsynaptic neuron, or a part of another type of cell such as a muscle cell. The synaptic terminals contain vesicles filled with chemicals called neurotransmitters. When the electrochemical signal moving down the axon reaches the synapse, the vesicles fuse with the membrane, and neurotransmitters are released, which diffuse across the synapse and bind to receptors on the membrane of the postsynaptic cell, potentially initiating a response in that cell. That response in the postsynaptic cell might include further propagation of an electrochemical signal to transmit information or contraction of a muscle fiber.

Extended description

(a) The neuron’s cell body (soma) holds the nucleus and gives rise to short, branching dendrites and one long axon. Oligodendrocytes form a myelin sheath that wraps most of the axon’s length, leaving small uncovered gaps called nodes of Ranvier at intervals; the axon ends at a synapse. (b) The synapse panel shows a presynaptic neuron above, releasing neurotransmitter-filled vesicles into the synaptic space; the neurotransmitters cross the gap and attach to receptors on the postsynaptic neuron below, the two neurons never touching.

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Meningitis and Encephalitis

Although the skull provides the brain with an excellent defense, it can also become problematic during infections. Any swelling of the brain or meninges that results from inflammation can cause intracranial pressure, leading to severe damage of the brain tissues, which have limited space to expand within the inflexible bones of the skull. The term meningitis is used to describe an inflammation of the meninges. Typical symptoms can include severe headache, fever, photophobia (increased sensitivity to light), stiff neck, convulsions, and confusion. An inflammation of brain tissue is called encephalitis, and patients exhibit signs and symptoms similar to those of meningitis in addition to lethargy, seizures, and personality changes. When inflammation affects both the meninges and the brain tissue, the condition is called meningoencephalitis. All three forms of inflammation are serious and can lead to blindness, deafness, coma, and death.

Meningitis and encephalitis can be caused by many different types of microbial pathogens. However, these conditions can also arise from noninfectious causes such as head trauma, some cancers, and certain drugs that trigger inflammation. To determine whether the inflammation is caused by a pathogen, a lumbar puncture is performed to obtain a sample of CSF. If the CSF contains increased levels of white blood cells and abnormal glucose and protein levels, this indicates that the inflammation is a response to an infection.

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Summary

• The nervous system consists of two subsystems: the central nervous system and peripheral nervous system.
• The skull and three meninges (the dura mater, arachnoid mater, and pia mater) protect the brain.
• Tissues of the PNS and CNS are formed of cells called glial cells and neurons.
• Since the blood-brain barrier excludes most microbes, there is no normal microbiota in the CNS.
• Some pathogens have specific virulence factors that allow them to breach the blood-brain barrier. Inflammation of the brain or meninges caused by infection is called encephalitis or meningitis, respectively. These conditions can lead to blindness, deafness, coma, and death.

Key terms

• peripheral nervous system (PNS) — network of neurons that connects the CNS with organs, sensory organs, and muscles throughout the body.
• central nervous system (CNS) — portion of the nervous system made up of the brain and spinal cord.
• meninges — membranes that surround the brain.
• dura mater — tough, outermost membrane that surrounds the brain.
• arachnoid mater — middle membrane surrounding the brain that produces cerebrospinal fluid. (Source note: this section’s own text attributes CSF production to cells of the choroid plexus, not the arachnoid mater; the arachnoid mater instead bounds the CSF-filled subarachnoid space, along with the pia mater.)
• pia mater — fragile and innermost membrane layer surrounding the brain.
• cerebrospinal fluid (CSF) — sterile liquid produced in the brain that fills the subarachnoid space of the brain and spinal column.
• neuropathy — numbness or tingling sensation caused by damage to peripheral nerves.
• glial cells — assists in the organization of neurons, provides a scaffold for some aspects of neuron function, and aids in recovery from neural injury.
• neurons — specialized cell found throughout the nervous system that transmits signals through the nervous system using electrochemical processes.
• soma — cell body of a neuron.
• dendrites — branched extensions of the soma of a neuron that interact with other cells.
• axon — long projection of a neuron along which an electrochemical signal is transmitted.
• myelin sheath — insulating layer that surrounds the axon of some neurons and helps to promote signal propagation.
• synapses — junction between a neuron and another cell.
• neurotransmitters — compound that is released at the synapse of neurons to stimulate or suppress the actions of other cells.
• meningitis — inflammation of the meningeal membranes that surround the brain.
• encephalitis — inflammation of the tissues of the brain.
• meningoencephalitis — inflammatory response that involves both the brain and the membranes that surround it.

Practice

Describe the major anatomical features of the nervous system

Explain why there is no normal microbiota of the nervous system

Explain how microorganisms overcome defenses of the nervous system to cause infection

Identify and describe general symptoms associated with various infections of the nervous system

This section is adapted from Microbiology, Section 26.1: Anatomy of the Nervous System by Nina Parker, Mark Schneegurt, Anh-Hue Thi Tu, Philip Lister, Brian M. Forster, and OpenStax, © OpenStax, licensed under CC BY-NC-SA 4.0. Access the original for free at openstax.org. Changes: the source’s garbled “an infectioninflinin” at the end of the Meningitis and Encephalitis section’s second paragraph is corrected to “an infection” (a one-word source defect); the Blood-Brain Barrier subsection’s Dionna Williams passage carries three further one-word source defects, each corrected in place without an inline note — “Johns Hopkin’s” to “Johns Hopkins’,” “studies the impact” to “study the impact” (subject-verb agreement with the plural “Researchers”), and “Williams also researchers the mechanisms” to “Williams also researches the mechanisms”; all four vendored figures (NervSys, Meninges, Neruron, and the ArtConnect neuron) are re-encoded as WebP and rendered as mediafigures after image inspection, each set kind="diagram" (overriding the media manifest’s photo guess, since every one of them is genuinely drawn line art, not a photograph or micrograph); the NervSys figure carries eager="true" as the page’s first figure; the Meninges and Neruron alts are rewritten under the 600-character cap with a longdesc walk-through added for each, since the source alts run long for what a caption alone can carry; the Link to Learning box’s anchor text is expanded from “video” to “this video about the blood-brain barrier” so the link names its own destination, its URL kept unchanged; the module’s two footnote citations (Yuki 2012, Cao-Lormeau 2016), neither of which carries a URL or a DOI in the CNXML, are rendered as inline parenthetical citations inside the Micro Connections box exactly as printed; the Clinical Focus box is titled Part 1, and its closing “Jump to the next Clinical Focus box” link is replaced with a sentence naming where the case continues, Acellular Diseases of the Nervous System (26.2 carries no Clinical Focus box in this chapter’s chain); its own three closing questions stay inside the callout as unanswered plain bullets; the section’s five source Multiple Choice items and five source Fill in the Blank items keep their source options, order, and keys unchanged (the two-blank Fill in the Blank keyed “blood-brain barrier” is rendered as one textin spanning both printed blanks, and grades correctly with no accept list needed, since hyphen-versus-space and case are already folded by the grader); the module’s one Matching exercise (four rows) is the first Matching set this book has shipped — per this book’s Matching rule, each of its four lettered descriptions becomes its own multiplechoice whose options are all four terms in the table’s own order, keyed by the source’s letter-to-term resolution (D, C, A, B read against the printed term order); the source table itself carries no data summary (summary="No Summary" is a layout placeholder, not a transcribable table), so no Markdown table duplicates it in the body; the section’s one Short Answer question bearing the exercise image (OSC_Microbio_26_01_ArtConnect_img, source prints no key) is rendered as a mediafigure, an author-written caption (the source prints none), one figure-keyed multiplechoice asking what letter E marks — keyed “myelin sheath” from the module’s own myelin-sheath sentence — and a selfcheck carrying the source’s full labeling question verbatim, its model answer walking the letter-to-structure mapping the vendored image actually draws (A soma, B axon, C a dendrite, D the synapse, E the myelin sheath); the source’s own exercise-image alt claims additional labels “F” (gaps) and “G” (dendrites) and describes the myelin sheath as “made from” structure C, none of which the printed artwork carries — the artwork instead draws exactly five lettered points (A–E), matching this book’s own labeled twin figure (OSC_Microbio_26_01_Neruron), where the same lower-left branch cluster is labeled “dendrite” and “oligodendrocyte” points elsewhere entirely — a source alt-vs-image defect; the section’s other two Short Answer questions and its one Critical Thinking question remain self-checks, since none is fixed by a single module sentence, with model answers and rubrics assembled only from this module’s own text; no source exercise, table, or Check Your Understanding bullet is omitted; of this section’s five body Check Your Understanding bullets (three boxes), one — the blood-brain barrier’s primary function — is graded as a multiplechoice, keyed verbatim by the module’s own one-sentence statement of that function, with distractors built from this module’s own sibling facts (CSF production by the choroid plexus, the aponeurosis’s anchoring role, and neurotransmitter signaling) that are true of the module but false as answers to this question; the remaining four (glial cells and their function; the structure and function of a synapse; the two types of CNS inflammation; why both forms of inflammation are so serious) remain self-checks, since each needs more than one module sentence assembled honestly; three fillers of two kinds are added to bring the second and fourth objective groups to this book’s three-item floor — one select-the-term multiplechoice built from the Summary’s own “no normal microbiota” sentence (second objective), and two textin text-recall items, “meningitis” and “meningoencephalitis,” each built from a single body sentence of this module (fourth objective) — disclosed here and in the source ledger; key terms are compiled from the module’s 19 <term> elements (no repeats), all 19 definitions taken directly from the book’s Glossary appendix, with no sentence-derived definitions needed; the Key terms bullet for “arachnoid mater” keeps the Glossary appendix’s wording but carries a visible Source note, since this section’s own body attributes CSF production to the choroid plexus rather than the arachnoid mater, which instead bounds the CSF-filled subarachnoid space — a claim correction, disclosed in place.