CNRN Exam

The chapters move from the cell to the whole patient: neurons, glia, the meninges, CSF and the blood-brain barrier; the functional anatomy of the brain, cranial nerves and spinal cord; cerebral blood flow and intracranial dynamics; and finally the bedside assessment tools and diagnostic studies that neuroscience nurses use every shift. Treat this section as the reference you return to whenever a later chapter mentions a tract, a territory or a test.

This chapter covers the cellular building blocks of the nervous system, how electrical and chemical signals travel, the protective coverings of the brain and spinal cord, the production and flow of cerebrospinal fluid, and the blood-brain barrier.

The neuron is the signaling cell of the nervous system. It has a cell body (soma) containing the nucleus, dendrites that receive input, and a single axon that carries the impulse away to the axon terminals. Many axons are wrapped in myelin, which insulates the axon and allows saltatory conduction, in which the impulse jumps between gaps called nodes of Ranvier. Myelinated fibers conduct much faster than unmyelinated fibers, which is why demyelinating diseases slow or block conduction.

Neurons are classified by function as sensory (afferent), motor (efferent) or interneurons, and by shape as multipolar, bipolar or unipolar. Mature neurons have very limited ability to divide, so neuronal death is largely permanent, while recovery depends on plasticity, in which surviving networks take over lost functions.

Glial cells outnumber neurons and support them. Their functions explain many disease patterns covered later in the guide.

Major Glial Cells and Their Clinical Relevance

Memory Aid: "Schwann in the Periphery, Oligo in the Center." Peripheral myelin (Schwann) is attacked in Guillain-Barre syndrome; central myelin (oligodendrocytes) is attacked in multiple sclerosis. Peripheral nerves can regenerate slowly along Schwann cell tubes; central axons rarely do.

At rest a neuron has a membrane potential of about -70 mV, maintained by the sodium-potassium pump (three sodium ions out, two potassium ions in) and by membrane permeability to potassium. When a stimulus raises the membrane to threshold, voltage-gated sodium channels open and sodium rushes in, causing depolarization. Potassium channels then open and potassium moves out, causing repolarization, often with a brief hyperpolarization. During the absolute refractory period no new impulse can fire; during the relative refractory period a stronger stimulus is needed.

These steps explain several drug actions. Many antiseizure drugs, such as phenytoin, carbamazepine and lamotrigine, stabilize voltage-gated sodium channels. Local anesthetics block sodium channels. Hyperkalemia and hypokalemia change membrane excitability, and severe hyponatremia causes cerebral edema and seizures because water shifts into brain cells.

At the synapse, the arriving impulse opens calcium channels in the axon terminal, triggering release of neurotransmitter into the synaptic cleft. The transmitter binds receptors on the next cell and is then removed by reuptake, enzymatic breakdown or diffusion.

Key Neurotransmitters

Excitotoxicity is a core concept in secondary brain injury. When neurons lose energy supply, glutamate floods the synapse, calcium pours into cells and triggers enzymes and free radicals that destroy the cell. This cascade is the reason the minutes and hours after a stroke or brain injury matter so much.

Three membranes cover the brain and spinal cord. From outside in, they are the dura mater, the arachnoid mater and the pia mater. The dura is tough and has folds: the falx cerebri separates the hemispheres and the tentorium cerebelli separates the cerebrum from the cerebellum. Structures above the tentorium are supratentorial; those below are infratentorial (brainstem and cerebellum, the posterior fossa).

Meningeal Spaces and Bleeding Patterns

Memory Aid: "PAD" from inside out: Pia, Arachnoid, Dura. The pia hugs the brain like plastic wrap.

The choroid plexus, mostly in the lateral ventricles, produces about 500 mL of cerebrospinal fluid per day, while only about 150 mL circulates at any time. The volume therefore turns over roughly three times a day. CSF cushions the brain, removes waste and helps buffer changes in intracranial volume.

The flow pathway is: lateral ventricles, through the foramina of Monro, into the third ventricle, through the cerebral aqueduct (of Sylvius) into the fourth ventricle, then out through the foramina of Luschka and Magendie into the subarachnoid space around the brain and spinal cord. CSF is absorbed mainly by the arachnoid granulations (villi) into the dural venous sinuses.

Production in the choroid plexus of the lateral ventricles.

Foramina of Monro to the third ventricle.

Cerebral aqueduct to the fourth ventricle.

Foramina of Luschka and Magendie to the subarachnoid space.

Absorption through arachnoid granulations into the venous sinuses.

Blockage anywhere within the ventricles causes obstructive (noncommunicating) hydrocephalus; failure of absorption at the arachnoid granulations, for example after subarachnoid blood or meningitis, causes communicating hydrocephalus.

Normal CSF is clear and colorless, with an opening pressure of roughly 10 to 20 cm H2O in an adult lying on the side, a protein of about 15 to 45 mg/dL, a glucose about 60% of serum glucose, and few or no white cells (0 to 5 lymphocytes per microliter).

Exam Tip: Expect questions linking CSF findings to diagnoses. Bacterial meningitis shows high neutrophils, high protein and low glucose; viral meningitis shows lymphocytes, mildly raised protein and normal glucose; Guillain-Barre syndrome shows high protein with a normal cell count.

The blood-brain barrier is formed by tight junctions between capillary endothelial cells, supported by astrocyte foot processes. It lets lipid-soluble substances, oxygen, carbon dioxide and glucose (by carrier) cross easily while blocking many drugs, proteins and pathogens. The barrier is weak or absent in a few areas, such as the area postrema (the vomiting center) and parts of the hypothalamus that sense blood osmolality.

Clinically, the barrier explains why some antibiotics penetrate poorly unless the meninges are inflamed, why mannitol works (it stays in the vessels and pulls water out of brain tissue when the barrier is intact), and why tumors and abscesses enhance with contrast (the barrier is disrupted). Barrier breakdown produces vasogenic edema, which responds to dexamethasone, unlike the cytotoxic edema of stroke and TBI, which does not.

Common Trap: Dexamethasone is not given for the cytotoxic swelling of ischemic stroke or traumatic brain injury. It is reserved for vasogenic edema around tumors and abscesses and as an adjunct in selected bacterial meningitis.

Myelin speeds conduction; CNS myelin comes from oligodendrocytes and PNS myelin from Schwann cells.

Excitotoxicity from glutamate and calcium influx drives secondary injury after stroke and trauma.

Epidural bleeds are usually arterial, subdural bleeds venous, and subarachnoid bleeds lie within the CSF space.

About 500 mL of CSF is made daily, about 150 mL circulates, and it is absorbed through arachnoid granulations.

Blood-brain barrier disruption causes vasogenic edema, which responds to steroids; cytotoxic edema does not.