Clinical Neuroanatomy Waxman

Ale Rmz

Clinical Neuroanatomy Waxman

Ale Rmz

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Abstract

27 ed

Figures (508)

» Numerous tables that make information clear and easy to remember

FIGURE 1-1 The structure of the central nervous system and the peripheral nervous system, showing the relationship between the central nervous system and its bony coverings.

FIGURE 1-2 The two major divisions of the central nervous sys- tem, the brain and the spinal cord, as seen in the midsagittal plane.

FIGURE 1-3 Cross section through the spinal cord, showing gray matter (which contains neuronal and glial cell bodies, axons, dendrites, and synapses) and white matter (which contains myelinated axons and associated glial cells). ( Reproduced, with permission, from Junqueira LC, Carneiro J Kelley RO: Basic Histology: Text & Atlas, 11th ed. McGraw-Hill, 2005.)

FIGURE 1-4 Photograph of a midsagittal section through the head and upper neck, showing the major divisions of the central nervous system. (Reproduced, with permission, from deGroot J: Correlative Neu- roanatomy of Computed Tomography and Magnetic Resonance Imagery. 21st ed. Appleton & Lange, 1991.)

FIGURE 1-5 Magnetic resonance image of a midsagittal section through the head (short time sequence; see Chapter 22). Compare with Figure 1-2.

FIGURE 1-6 Planes (coronal, horizontal, transverse) and direc- tions (rostral, caudal, etc.) frequently used in the description of the brain and spinal cord. The plane of the drawing is the midsagittal.

FIGURE 2-3 Schematic drawing of a Nissl-stained motor neuron. The myelin sheath is produced by oligodendrocytes in the central nervous system and by Schwann cells in the peripheral nerv- ous system. Note the three motor end-plates, which transmit the nerve impulses to striated skeletal muscle fibers. Arrows show the direction of the nerve impulse. (Reproduced, with permission, from Junqueirz LC, Carneiro J, Kelley RO: Basic Histology: Text &Atlas, 11th ed. McGraw-Hill, 2005.)

FIGURE 2-2 = Schematic illustration of nerve cell types. A: Central nervous system cells: (1) motor neuron projecting to striated muscle, (2) special sensory neuron, and (3) general sensory neuron from skin. B: Autonomic cells to smooth muscle. Notice how the po- sition of the cell body with respect to the axon varies. projections that act as fine dendritic branches and receive synaptic inputs (Fig 2-5). Dendritic spines are currently of great interest to researchers. The shape of a spine regulates the strength of the synaptic signal that it receives. A synapse onto the tip of a spine with a thin “neck” will have a smaller influ- ence than a synapse onto a spine with a thick neck. Dendritic spines are dynamic, and their shape can change. Changes in dendritic spine shape can strengthen synaptic connections so as to contribute to learning and memory. Maladaptive changes

FIGURE 2-1 Twostages in the development of the neural tube (only half of each cross section is shown). A: Early stage with large central canal. B: Later stage with smaller central canal.

FIGURE 2-4 Electron micrograph of a nerve cell body (CB) surrounded by nerve processes. The neuronal surface is completely cov- ered by either synaptic endings of other neurons (S) or processes of glial cells. Many other processes around this cell are myelinated axons (M). CB, neuronal cell body; N, nucleus, X 5000. (Courtesy of Dr.DM McDonald.)

FIGURE 2-5 _ Dendrite from pyramidal neuron in the motor cor- tex. Note the spines on the main dendrite and on its smaller branches. Scale = 10 um. (Micrograph courtesy of Dr. Andrew Tan, Yale University.)

FIGURE 2-/ Diagrammatic view, in three dimensions, of a prototypic neuron. Dendrites (1) radiate from the neuronal cell body, which contains the nucleus (3). The axon arises from the cell body atthe initial segment (2). Axodendritic (4) and axosomatic (5) synapses are present. Myelin sheaths (6) are present around some axons. Transmission of information between neurons occurs at synapses. Communication between neurons usually occurs from the axon terminal of the transmitting neuron (presyn- aptic side) to the receptive region of the receiving neuron (postsynaptic side) (Figs 2-7 and 2-12). This specialized in- terneuronal complex is a synapse, or synaptic junction. As outlined in Table 2-1, some synapses are located between an axon and a dendrite (axodendritic synapses, which tend to be excitatory), or a thorn, or mushroom-shaped dendritic spine

FIGURE 2-6 Micrographs showing dendrites of dorsal horn neurons from a normal rat (A) and from a rat following nerve injury (B). Note the increased number of dendritic spines and their altered shape following nerve injury. Bar = 10 jum. (Modified from Tan AM et al: Racl-regulated dendritic spine remodeling contributes to neuropathic pain after peripheral nerve injury, Exper Neurol 2011;232:222-233.)

FIGURE 2-8 A: in the peripheral nervous system (PNS), unmyelinated axons are located within grooves on the surface of Schwann cells. These axons are not, however, insulated by a myelin sheath. B: Myelinated PNS fibers are surrounded by a myelin sheath that is formed by a spiral wrapping of the axon by a Schwann cell. Panels 1-4 show four consecutive phases of myelin formation in peripheral nerve fibers. (Reproduced, with permission, from Junqueira LC, Carneiro J, Kelley RO: Basic Histology, 11th ed. McGraw-Hill, 2005.)

Macroglia roles, including myelin formation, guidance of developing neurons, maintenance of extracellular K* levels, and reup- take of transmitters after synaptic activity. There are two broad classes of glial cells, macroglia and microglia (Table 2-2).

TABLE 2-2 Nomenclature and Principal Functions of Glial Cells.

FIGURE 2-10 Oligodendrocytes form myelin in the central nervous system (CNS). A single oligodendrocyte myelinates an en- tire family of axons (2-50). There is little oligodendrocyte cytoplasm (Cyt) in the oligodendrocyte processes that spiral around the axon to form myelin, and the myelin sheaths are connected to their par- ent oligodendrocyte cell body by only thin tongues of cytoplasm. This may account, at least in part, for the paucity of remyelination after damage to the myelin in the CNS. The myelin is periodically interrupted at nodes of Ranvier, where the axon (A) is exposed to the extracellular space (ES). (Redrawn and reproduced with permission from Bunge M, Bunge R, Pappas G: Ultrastructural study of remyelination in an experimen- tal lesion in adult cat spinal cord, J Biophys Biochem Cytol May;10:67-94, 1961.)

FIGURE 2-11 Electron micrograph showing oligodendrocyte (OL) in the spinal cord, which has myelinated two axons (A ,, A,). X 6600. The inset shows axon A, and its myelin sheath at higher magnification. The myelin is a spiral of oligodendrocyte membrane that surrounds the axon. Most of the oligodendrocyte cytoplasm is extrudedfrom the myelin. Because the myelin is compact, it has a high electrica resistance and low capacitance so that it can function as an insulator around the axon. X 16,000.

TiIwWwWNe a2” '4 SRTICTIGACIL CAVITY UF & SYTIGP Ue LOE EEtertcls. Vesicles fuse with the presynaptic membrane and release transmitter molecules into the synaptic cleft so that they can bind to receptors in the postsynaptic membrane.

FIGURE 2-13 Axodendritic synapses terminate on dendri- ties or mushroom-shaped “dendritic spines,’ and tend to be exci- tatory. Axosomatic synapses terminate on neuronal cell bodies and tend to be inhibitory. Axoaxonal synapses terminate on an axon, often close to synaptic terminals, and modulate the release of neuro- transmitters. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.)

FIGURE 2-14 Light micrograph of a small group of neurons (nucleus) in a network of fibers (neuropil). X800. Bielschowsky silver stain.

FIGURE 2-15 Micrographs showing astrocytes within the nor- mal human brain (A), and within glial scars in patients with multiple sclerosis (B) and following stroke (C). Note the hypertrophied astrocytes within glial scars in (B) and (C). Bar = 10 pum. (Courtesy of Dr. Joel Black, Yale University School of Medicine.) The cell body maintains the functional and anatomic integrity of the axon (Fig 2-16). If the axon is cut, the part distal to the cut degenerates (wallerian degeneration), because materials for maintaining the axon (mostly proteins) are formed in the cell body and can no longer be transported down the axon (axoplasmic transport).

FIGURE 2-16 Main changes that take place in an injured nerve fiber. A: Normal nerve fiber, with its perikaryon and the effector cell (striated skeletal muscle). Notice the position of the neuron nucleus and the amount and distribution of Nissl bodies. B: When the fiber is injured, the neuronal nucleus moves to the cell periphery, Niss] bodies become greatly reduced in number (chromatolysis), and the nerve fiber distal to the injury degenerates along with its myelin sheath. Debris is phagocytized by macrophages. C: The muscle fiber shows pronounced disuse atrophy. Schwann cells proliferate, forming a compact cord that is penetrated by the growing axon. The axon grows at a rate of 0.5 to 3 mm/d. D: In this example, the nerve fiber regeneration was successful, and the muscle fiber was also regenerated after receiving nerve stimuli. E: When the axon does not penetrate the cord of Schwann cells, its growth is not organized and successful regenera tion does not occur. (Redrawn and reproduced, with permission, from Willis RA, Willis AT: The Principles of Pathology and Bacteriology, 3rd ed. Butterworth, 1972.)

FIGURE 2-17 Summary of changes occurring in a neuron anc the structure it innervates when its axon is crushed or cut at the point marked X. (Modified from Ries D. Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.)

TABLE 3-1 Concentration of Some Ions Inside and Outside Mammalian Spinal Motor Neurons. Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 18th ed. Appleton & Lange, 1997. Data from Mommaerts WFHM, in: Essentials of Human Physi- ology. Ross G (editor). Year Book, 1978.

FIGURE 3-1 Na* and K* flux through the resting nerve cell membrane. Notice that the Na*/K* pump (Na‘/K*-ATPase) tendsto extrude Na* from the interior of the cell, but it carries K* ions inward. (Reproduced, with permission, from Eccles JC: The Physiology of Nerve Cells. Johns Hopkins University Press, 1957.)

FIGURE 3-2 Demonstration of a generator potential in a pacinian corpuscle. The electrical responses to a pressure (black arrow) of 1X, 2X, 3X, and 4X are shown. The strongest stimulus produced an action potential in the sensory nerve, originating in the center of the corpuscle (open arrow).

FIGURE 3-4 Ionic basis for the depolarization underlying the action potential. Voltage-sensitive Na* channels open when the membrane is depolarized. This action results in increased Na* permeability of the membrane, causing further depolarization and the opening of still other Na* channels. When a sufficient number of Na* channels have opened, the membrane generates an explosive, all-or-none depolarization—the action potential. Other voltage-sensitive ion channels (voltage- sensitive K* channels) open (usually more slowly than Na* channels) in response to depolarization and are selectively

In some fibers, membrane potential becomes transiently hyperpolarized (the after-hyperpolarization) as a result of the opening of the K* channels, which tends to drive the mem- brane toward Ex. In the wake of an action potential, there is a refractory period of decreased excitability. This period has two phases: the initial absolute refractory period, during which

permeable to K*. When these channels open, the membrane potential is driven toward the K* equilibrium potential (Ex), leading to hyperpolarization.

FIGURE 3-6 Na‘ and K‘ channel distributions in myelinated axons are not uniform. Na* channels (gy) are clustered in high density in the axon membrane at the node of Ranvier, where they are available to produce the depolarization needed for the action poten- tial. K* channels (g,), on the other hand, are located largely in the in- ternodal axon membrane under the myelin, so that they are masked. (Reproduced with permission from Waxman SG: Membranes, myelin and the patho- physiology of multiple sclerosis, NEng/J Med Jun 24;306(25):1529-33, 1982.) contrary, it is periodically interrupted by small gaps (approxi- mately 1 um long), called the nodes of Ranvier, where the axon is exposed. In mammalian myelinated fibers, the voltage-sensi- tive Na* and K* channels are not distributed uniformly. Na* channels are clustered in high density (about 1000/pm”) in the axon membrane at the node of Ranvier, but are sparse in the in- ternodal axon membrane, under the myelin. K* channels, on the other hand, tend to be localized in the “internodal” and “paranodal” axon membrane, that is, the axon membrane cov- ered by the myelin (Fig 3-6).

FIGURE 3-7 A: Saltatory conduction in a myelinated axon. The myelin functions as an insulator because of its high resistance and low ca- pacitance. Thus, when the action potential (cross-hatching) is at a given node of Ranvier, the majority of the electrical current is shunted t o the next node (along the pathway shown by the broken arrow). Conduction of the action potential proceeds in a discontinuous manner, jumping from node to node witha high conduction velocity. B: In demyelinated axons there is loss of current through the damaged myelin. Asa result, it either takes longer to reach threshold and conduction velocity is reduced, or threshold is not reached and the action potential fails to propa- gate. (Reproduced, with permission, from Waxman SG: Membranes, myelin and the pathophysiology of multiple sclerosis. N Engl JMed 1982;306:1529.)

FIGURE 3-8 Relationship between conduction velocity and di- ameter in myelinated and nonmyelinated axons. Myelinated axons conduct more rapidly than nonmyelinated axons of the same size.

TABLE 3-2 Nerve Fiber Types in Mammalian Nerve. Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.

FIGURE 3-9 Atrophy (loss of muscle mass) in the hands of a patient with hereditary sensorimotor neuropathy. Peripheral neuropathies affect the longest nerve fibers first, and the f eet and hands thus are affected in early stages of the disease. (Courtesy of Dr. Catherina Faber.)

TABLE 3-5 Areas of Concentration of Common Neurotransmitters.

Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hiil, 2005. TABLE 3-3 Numeric Classification Sometimes Used for Sensory Neurons.

FIGURE 3-1U Schematic representation of some of the events involved in neurotransmitter synthesis, release, and action at a prototypic synapse, the neuromuscular junction. Acetylcholine (ACh) is the transmitter at this synapse. Part of the nerve terminal is shown, lying in close apposition to a muscle end- plate. Synthesis of ACh occurs locally, in the presynaptic t erminal, from acetyl-coenzyme A (CoA) and choline (1). ACh is then incorpo- rated into membrane-bound synaptic vessels (2). Release of ACh oc- curs by exocytosis, which involves fusion of the vesicles with the presynaptic membrane (3). This process is triggered by an influx of Ca?*, which occurs in response to propagation of the action poten- tial into the presynaptic axons. The contents of approximately 200 synaptic vesicles are released into the synaptic cleft in response toa single action potential. The released ACh diffuses rapidly across the synaptic cleft (4) and binds to postsynaptic ACh receptors (5), where it triggers a conformational change that leads to an influx of Na* ions, which depolarizes the membrane. When the channel closes, the ACh dissociates and is hydrolyzed by acetylcholinesterase (6). (Reproduced, with permission, from Murray RK, Granner DK, Mayes PA, Rodwell VW Harper's Biochemistry, 24th ed. Appleton & Lange, 1996.)

*Directly linked receptors do not use second messengers. Data from Ganong WF Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005. TABLE 3-6 Common Neurotransmitters and Their Actions.

FIGURE 3-11 Top: Schematic illustration of two types of inhi- bition in the spinal cord. In direct inhibition (also called postsynaptic inhibition), a chemical mediator released from an inhibitory neuron causes hyperpolarization (inhibitory postsynaptic potential) of a motor neuron. In presynaptic inhibition, a second chemical media- tor released onto the ending (axon) of an excitatory neuron causes a reduction in the size of the postsynaptic excitatory potential. Bottom: Diagram of a specific inhibitory system involving an inhibitory interneuron (Renshaw cell).

FPIMUNE os-te ochnematic iiustrations of a myoneural junc- tion. A: Motor fiber supplying several muscle fibers. B: Cross section as seen in an electron micrograph.

FIGURE 4-1 Magnetic resonance image (MRI) of a 51-year-olc patient with hypertension. The patient complained of weakness of the right side of the face and the right arm and leg, which had devel- oped over a 5-h period. There was no sensory loss or problems with language or cognition. The MRI revealed a small infarction in the in- ternal capsule (arrow), which destroyed axons descending from the motor cortex, thus causing a “pure motor stroke” in this patient.

FIGURE 4-2 A: Section through the medulla, stained for myelin, from a patient with multiple sclerosis. Notice the multiple demyelinated plaques (labeled 1-4) that are disseminated throughout the central nervous system ( CNS). B: Even a single lesion can interfere with function in multiple neighboring parts of the CNS. Notice that plaque 3 involves the hypoglossal r oot (producing weakness of the tongue) and the medial lemnisci (causing an impairment of vibratory and t ouch-pressure sense). Figure 7—7B shows, for comparison, a diagram of the normal medulla at this level. meiosis; impairment of all sensory modalities over the ipsilat- eral face; and loss of pain and temperature sensitivity over the contralateral torso and limbs. This syndrome results from dys- function of clustered nuclei and tracts in the lateral medulla and is usually due to infarction resulting from occlusion of the posterior inferior cerebellar artery, which irrigates these neighboring structures.

TABLE 4-1 Mechanisms Leading to Dysfunction in Typical Neurologic Diseases. CNS, central nervous system;CSF, cerebrospinal fluid.

FIGURE 4-3 Computed tomography scan showing astroke in the territory of the middle cerebral artery. Multifocal Process: Multifocal pathology results in dam- age to the nervous system at numerous separate sites. In mul- tiple sclerosis, for example, lesions are disseminated through- out the nervous system in the spatial domain, and develop at different points in time. Figure 4-2 shows the multifocal nature of the pathology in a patient with multiple sclerosis.

FIGURE 4-4 As: Pyramidal tract. B: Dorsal column system. C: Spinothalamic system.

FIGURE 4-5 Characteristic time courses for various neurologic disorders. A: Brief episodes of dysfunction may represent seizures or migraine attacks. B: A pattern of recent-onset headaches on wakening may be caused by an expanding brain tumor. C: A relapsing-remitting course is characteristic of multiple sclerosis. D: Sudden onset of a fixed deficit is characteristic of cerebrovascular disease. E: Slowly progressive dysfunction is suggestive of neurodegenerative diseases, such as Alzheimer’s or Parkinson’s. F: Subacutely progressive dysfunction, which advances over weeks to months, is often seen with brain tumors.

FIGURE 5-1 Schematic cross sections (A-F) showing the devel- opment of the spinal cord.

FIGURE 5-2 Cross section showing two phases in the devel- opment of the spinal cord (each half shows one phase). A: Early phase. B: Later phase with central cavity.

FIGURE 5-4 Schematic illustration of the relationships between the vertebral column, the spinal cord, and the spinal nerves. Note the mismatch between the location of spinal cord segments and of vertebral level where roots exit from the vertebral column. Note also the termination of the spinal cord at the level of theL1 or L2 vertebral body.

FIGURE 5-3 Schematic dorsal view of isolated spinal cord and spinal nerves.

TABLE 5-1 Anatomic Relationships of Spinal Cord and Bony Spine in Adults. SPINAL ROOTS AND NERVES

FIGURE 5-5 Anatomy of the spinal cord shown in cross section. Note that the terms “dorsal” and “posterior” are used interchangeably and that “ventral” and “anterior” are also used inter- changeably to describe the spinal cord.

FIGURE 5-8 Segmental distribution of the body viewed in the approximate quadruped position.

FIGURE 5-9 Diagram of the position of the nipple in the sen- sory skin fields of the third, fourth, and fifth thoracic spinal roots showing the overlapping of the cutaneous areas. The term myotome refers to the skeletal musculature innervated by motor axons in a given spinal root. The organization of my- otomes is the same from person to person, and the testing of motor functions (see Appendix B) can be very useful in deter- mining the extent of a lesion in the nerve, spinal cord segment, or tract, especially when combined with a careful sensory examina- tion. Most muscles, as indicated in Appendix B, are innervated by

FIGURE 5-11 _Laminas of the gray matter of the spinal cord (only one-half shown). 6. Lamina VIl—This is a large zone that contains the cells of the dorsal nucleus (Clarke’s column) medially as well as a large portion of the ventral gray column. Clarke’s column con- tains cells that give rise to the posterior spinocerebellar tract. Lamina VII also contains the intermediolateral nucleus (or intermediolateral cell column) in thoracic and upper lumbar regions. Preganglionic sympathetic fibers project from cells in this nucleus, via the ventral roots and white rami communi- cantes, to sympathetic ganglia.

FIGURE 5-10 Transverse sections of the spinal cord at various levels.

FIGURE 5-12 Diagram showing the functional localization of motor neuron groups in the ventral gray horn of a lower cervical seg- ment of the spinal cord.

FIGURE 5-13 Schematic illustration of the course of corticospinal tract fibers in the spinal cord, together with cross sections at represen- tative levels. This and the following schematic illustrations show the cord in an upright position.

TABLE 5-3 Descending Fiber Systems in the Spinal Cord. F. Tectospinal Tract neurons in the thoracolumbar spinal cord (lateral column) and to preganglionic parasympathetic neurons in sacral seg- ments (see Chapter 20). Descending fibers in this system modulate autonomic functions, such as blood pressure, pulse and respiratory rates, and sweating.

TABLE 5-4 Ascending Fiber Systems in the Spinal Cord.

FIGURE 5-16 The spinothalamic (ventrolateral) system in the spinal cord.

The dorsal nucleus of Clarke is not present above C8; it is replaced, for the upper extremity, by a homologous nucleus called the accessory cuneate nucleus. Dorsal root fibers origi- nating at cervical levels synapse with second-order neurons in the accessory cuneate nucleus.

FIGURE 5-18 _ Diagram illustrating the pathways responsible for the stretch reflex and the inverse stretch reflex. Stretch stimulates the muscle spindle, and impulses pass up the la fiber to excite the lower (alpha) motor neuron. Stretch also stimulates the Golgi tendon organ, which is arranged in series with the muscle, and impulses passing up the |b fiber activate the inhibitory neuron. With strong stretch, the re- sulting hyperpolarization of the motor neuron is so great that it stops discharging. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.)

TABLE 5-6 __Lower- Versus Upper-Motor-Neuron Lesions.

FIGURE 5-21 Schematic illustration of ipsilateral and crossed polysynaptic reflexes.

FIGURE 5-22 Motor pathways divided into upper- and lower- motor-neuron regions.

FIGURE 5-23 Testing for extensor plantar reflexes.

FIGURE 5-27 Wasting of the small muscles of the hands in a woman with syringomyelia.

FIGURE 5-25 Brown-Séquard syndrome with lesion at left tenth thoracic level (motor deficits not shown).

FIGURE 5-26 Syringomyelia involving the cervicothoracic por- tion of the spinal cord.

FIGURE 6-1 Schematic illustration of the relationships between the spinal cord, spinal nerves, and vertebral column (lateral view), showing the termination of the dura (dura mater spinalis) and its con- tinuation as the filum terminale externum. (Compare with Fig 5-4.)

FIGURE 6-4 Cross section of the cervical spinal cord. The diagram shows the anterior and posterior spinal arteries with their branches and territories. There are numerous variations in the vascu- lar supply.

FIGURE 6-3 Epidural tumor in Hodgkin's disease, showing compression of the thoracic spinal cord (Weil stain). The illustration is positioned to conform with customary CT and MR imaging procedures.

FIGURE 6-5 Vascularization of the spinal cord (ventral view).

FIGURE 6-7 Computed tomography image of a horizontal sec- tion at midlevel of vertebra L4. done with the patient sitting upright, the fluid in the manometer normally rises to about the level of the midcervi- cal spine (Fig 6-10. Coughing, sneezing, or straining usually causes a prompt rise in pressure from the congestion of the spinal veins and the resultant increased pressure on the contents of the subarachnoid and epidural spaces. The pres- sure subsequently falls to its previous level.

FIGURE 6-8 Computed tomography image of a horizontal section through L4 at the level of the L3-4 intervertebral disk. (Repro- duced, with permission, from deGroot J: Correlative Neuroanatomy of Computed Tomography and Magnetic Resonance Imaging. 21st ed. Appleton & Lange, 1991.) After the initial pressure has been determined, three or four samples of 2-3 mL each are withdrawn into sterile tubes for laboratory examination. Routine examination usually in- cludes cell counts and measurement of total protein. Cultures and special tests, such as those for sugar and chlorides, are done when indicated. The pressure is also routinely measured after the fluid is removed.

FIGURE 6-10 Lumbar puncture site with the patient in sitting position. The approach to the sacral hiatus f or saddle-back anesthe- sia is also indicated.

FIGURE G-2 Decubitus position for lumbar puncture. (Reproduced, with permission, from Krupp MA et al: Physician’s Handbook, 21st ed. Appleton & Lange, 1985.)

FIGURE 6-12 Roentgenogram of lumbar vertebrae (left lateral view). (Compare with Fig 6-6, right side.)

FIGURE 6-11 Roentgenograms through the neck (lateral view). Information about the position, shape, and size of all the ele- ments of the spine, cord, roots, ligaments, and surrounding soft tissue can be obtained by a series of thin (0.15-1 cm) transverse (axial) CT images (or scans) (see Fig 6-7). CT myelography is done after contrast medium is injected into the subarachnoid space (Figs 6-13 and 6-14).

FIGURE 6-14. Reformatted CT image of midsagittal section of the lumbar spine of a patient who fell from a third-floor window. There is a compression fracture in the body of L1, and the lower cord is compressed between bony elements of L1 ( arrows). The subarachnoic space was injected with contrast medium. (Reproduced with permission from Federle MP, Brant-Zawadski M (editors): Computed tomography in the evalua- tion of trauma, 21st edition. Lippincott Williams & Wilkins, 1986.)

FIGURE 6-15 Magnetic resonance image of a coronal section through the body and (curved) lumbar spine. (Reproduced, with permission, fro deGroot J: Correlative Neuroanatomy of Computed Tomography and Magnetic Resonance Imaging. 21st ed. Appleton & Lange, 1991.) Magnetic resonance imaging can be used in any plane. It has been used, especially with sagittal images, to demonstrate the anatomy or pathology of the spinal cord and surrounding spaces and structures (Figs 6-15 to 6-18). Because the calcium of bone does not yield a magnetic resonance signal, MRI is especially useful in showing suspected lesions of the soft tissues in and around the vertebral column (Figs 6-16 and 6-19).

FIGURE 6-13 Computed tomography image of a horizontal section at the level of vertebra T12 in a 3-year-old child. The subarachnoid space was injected with contrast medium.

FIGURE 6-18 Magnetic resonance image of a sagittal section of the lumbosacral spine. The arrow heads point to an intervertebral disc herniation atthe L3-L4 level. (Reproduced, with permission, from Ami- noff MJ, Greenberg DA, Simon RP: Clinical Neurology, 6th ed. McGraw-Hill, 2005.)

FIGURE 6-16 Magnetic resonance image of a coronal section through the neckat the level of the cervical vertebrae. Because of the curvature of the neck, only five vertebral bodies are seen in this plane. (Reproduced, with permission, from Mills CM, deGroot J, Posin J: Magnetic Resonance Imaging Atlas of the Head, Neck, and Spine. Lea & Febiger, 1988.)

FIGURE 6-19 Magnetic resonance image of a midsagittal sec tion through the lumbosacral spine. The mass visible in the body of L4 represents a metastasis of a colon carcinoma (arrow).

FIGURE 6-17 Magnetic resonance image of a midsagittal sec- tion through the lower neck and upper thorax of a patient with AIDS. Multiple masses are seen in the vertebral bodies at several levels (arrows): Pathologic examination showed these to be malignant

FIGURE 7-1 Four stages in early development of brain and cranial nerves (times are approximate). A: 34 weeks. B: 44 weeks. C: 7 weeks. D: 11 weeks.

FIGURE 7-2 Schematic illustration of the widening of the central cavity in the lower brain stem during development.

-IGURE 7-3 Ventral view of the brain stem, in relation to cerebral hemispheres and cerebellum, showing the cranial nerves.

FIGURE 7-4 Drawing of the divisions of the brain stem in a midsagittal plane. The major internal longitudinal divisions are the tectum, tegmentum, and basis. The major external divisions are the midbrain, pons, and medulla.

FIGURE 7-5 Dorsolateral aspect of the brain stem (most of cerebellum removed).

TABLE 7-1 Major Ascending and Descending Pathways in the Brain Stem.

FIGURE 7-6 Cranial nerve nuclei. Left: Dorsal view of the human brain stem with the positions of the cranial nerve nuclei projected on the surface. Motor nuclei are on the left; sensory nuclei are on the right. Right: Transverse sections at the levels indicated by the arrows.

* The solitary nucleus is shared by nerves VII, IX, and X. * The ambiguus nucleus is shared by nerves IX, X, and XI. TABLE 7-2 Cranial Nerves and Nuclei in the Brain Stem.

The tegmentum of the pons is more complex than the base. The lower pons contains the nucleus of nerve VI (abducens nucleus) and the nuclei of nerve VII (the facial, superior sali- vatory, and gustatory nuclei). The branchial motor compo- nent of the facial nerve loops medially around the nucleus of nerve VI. The upper half of the pons harbors the main sensory nuclei of nerve V (Figs 7-7E and 7-8). The medial lemniscus assumes a different position (lower body, medial; upper body, lateral), and the spinothalamic tract courses even more later- ally as it travels through the pons.

FIGURE 7-9 Corticobulbar pathways to the nuclei of cranial nerves Vil and XII. Notice that the facial nucleus for muscles of the upper face receives descending input from the motor cortex on both sides, whereas the facial nucleus for lower facial muscles receives in- put from only the contralateral cortex.

FIGURE 7-10 Principal arteries of the brain stem (ventral view).

FIGURE 7-13 Clinical syndromes associated with midbrain lesions (compare with Fig 7-7G).

FIGURE 7-12 Clinical syndromes associated with pontine le- sions (compare with Fig 7-7D).

FIGURE 7-11 Clinical syndromes associated with medullary lesions (compare with Fig 7-7C). CEREBELLUM

FIGURE 7-14 Magnetic resonance image showing, in the sagittal plane, a mass lesion (arrow heads) in the patien described in Case Illustration 7-3. The mass lesion, which was shown on biopsy to be a germinoma, compressed the quadrigeminal plate and obstructed the cerebral aqueduct [arrow]. (Case illustration and image courtesy of Joachim Baehring, MD, Yale University School of Medicine.) This tragic case illustrates the locked-in syndrome. The in- farction, in the base of the pons, destroyed the corticospinal and corticobulbar tracts and thus produced paralysis of the limbs and bulbar musculature. Preservation of the oculomotor and trochlear nuclei and of their nerves permitted some

FIGURE 7-15 Midsagittal section through the cerebellum.

FIGURE 7-16 Cerebellar homunculi. Proprioceptive and tactile stimuli are projected as shown in the upper (inverted) homunculus and the lower (split) homunculus. The striped area represents the re- gion from which evoked responses to auditory and visual stimuli are observed. (Redrawn and reproduced, with permission, from Snider R: The cerebel- lum. Sci Am 1958;199:84.)

* Several other pathways transmit impulses from nuclei in the brain stem to the cerebellar cortex and to the deep nuclei. Data from Ganong WF: Review of Medical Physiology, 22nd ed. Appleton & Lange, 2005. ABLE 7-3 Functions and Major Terminations of the Principal Afferent Systems to the Cerebellum.*

FIGURE 7-17 Photomicrograph of a portion of the cerebellum Each lobule contains a core of white matter and a cortex consisting of three layers—granular, Purkinje, and molecular—of gray matter. H&E stain, X 28. (Reproduced, with permission, from Junqueira LC, Carneiro J, Kelley RO: Basic Histology, 8th ed. Appleton & Lange, 1995.)

-IGURE 7-19 Schematic diagram of the cerebellar cortex.

FIGURE 7-18 Photomicrograph of cerebellar cortex. This staining procedure does not reveal the unusually large dendritic arborization of the Purkinje cell. H&E stain, *250. (Reproduced, with per- mission, from Junqueira LC, Carneiro J, Kelley RO: Basic Histology, 8th ed. Appleton 8 Lange, 1995.)

FIGURE 7-20 Diagram of neural connections in the cerebellum. Shaded neurons are inhibitory. “+” and “—” signs indicate whether endings are excitatory or inhibitory. BC, basket cell; GC, Golgi cell; GR, granule cell; NC, cells within deep cerebellar nuclei; PC, Purkinje cell. Connections of the stellate cells are similar to those of the basket cells, except that they end, for the most part, on Purkinje cell dendrites. (Modified with permission from Ganong WF: Review of Medical Physiology, 22nd edition, McGraw-Hill, 2005.)

FIGURE 7-21 Schematic illustration of some cerebellar afferents and outflow pathways. FIGURE 7-22 Magnetic resonance images showing tumor (medulloblastoma), shown by white arrow, originating from midline cerebellar structures, in a 29-year-old man who had experienced headaches upon awakening f or a month. On examination, he was unable to tandem walk due to cerebellar dysfunction, and his deep tendon stretch reflexes were brisk, probably due to compression ofthe corticospinal tracts within the brain stem. Asa result of prompt diagnosis, there was complete recovery after craniospinal irradiation and chemotherapy. (Courtesy of Joachim M. Baehring, MD, DSc, Yale University School of Medicine.)

FIGURE 7-23 Magnetic resonance image of a coronal section through the head at the level of the fourth ventricle.

IGURE 8-1 Ventral view of the brain stem with cranial nerves.

TABLE 8-2 Ganglia Related to Cranial Nerves.

FIGURE 8-2 Lateral view of the olfactory bulb, tract, mucous membrane, and nerves.

FIGURE 8-3 Horizontal section through the head at the level of the orbits.

Reproduced, with permission, from Vaughan D, Asbury T, Riordan-Eva P: Genera Ophthalmology, 17th ed. Appleton & Lange, 2008. TABLE 8-3 Functions of the Ocular Muscles.

TABLE 8-4 Yoke Muscle Combinations. Reproduced, with permission, from Vaughan D,Asbury T, Riordan-Eva P: General Ophthalmology, 17th ed. Appleton & Lange, 2008.

FIGURE 8-6 Types of eye movement control. (Modified and repro- duced, with permission, from Robinson DA: Eye movement control in primates. Science 1968;161:1219. Copyright ©1968 by the American Association for the Advancement of Science.) The six individual muscles that move one eye normally act together with the muscles of the other eye in controlled movement. Both eyes move in the same direction to follow an object in space, but they move by simultaneously contracting and relaxing different muscles; this is called a conjugate gaze movement. Fixating on a single point is called vergence,

which requires a different set of muscles, including the in- traocular muscles. Each of the extraocular muscles is brought into play in conjugate gaze movements or vergence.

FIGURE 8-7 Brain circuitry controlling right conjugate gaze. The command for voluntary conjugate movements in right lateral gaze origi- nates in the frontal eye fields in the left frontal lobe. This command excites a lateral gaze control center, adjacent to the abducens nucleus, within the paramedian pontine reticular formation on the right side. This, in turn, activates the abducens nucleus on the right, turning the right eye to the right, and projects via the median longitudinal fasciculus to the oculomotor nucleus on the left, which turns the left eyet o the right. (Reproduced, with permission, from Aminoff ML, Greenberg DA, Simon RP: Clinical Neurology, 6th ed. McGraw-Hill, 2005.)

TABLE 8-5 Paralyses of Individual Eye Muscles.* * Diplopia is noted only when the affected eye attempts these movements.

FIGURE 8-9 The path of the pupillary light reflex.

FIGURE 8-10 _Left-sided oculomotor (third nerve) palsy in a patient with diabetes. There is failure of adduction of the left eye, ptosis of the left eyelid, and normal pupillary function. (Reproduced, with permission, from Riordan-Eva P, Witcher JP: Vaughan & Asbury’s General Ophthalmology, 17th ed. McGraw-Hill, 2008.)

FIGURE 8-12 Sensory distribution of nerve V. FIGURE 8-11 | The trigeminal nerve and its branches.

TABLE 8-6 Distribution of the Trigeminal Nerve.

The visceral afferent component of the nervus inter- medius, with cell bodies in the geniculate ganglion, carries taste sensation from the anterior two-thirds of the tongue via the chorda tympani to the solitary tract and nucleus. The so- matic afferent fibers from the skin of the external ear are car- ried in the facial nerve to the brain stem. These fibers connect

Cranial nerve VIII is a double nerve that arises from spiral and vestibular ganglia in the labyrinth of the inner ear (Fig 8-15). It passes into the cranial cavity via the internal acoustic meatus and enters the brain stem behind the poste- rior edge of the middle cerebellar peduncle in the pontocere- bellar angle. The cochlear nerve is concerned with hearing;

FIGURE 8-16 The glossopharyngeal nerve. TP, tympanum plexus; FR, foramen rotundum; FO, foramen ovale.

FIGURE 8-17 Sensory innervation of the tongue.

8-19 The vagus nerve. J, jugular (superior) ganglion; N, nodose (inferior) ganglion.

FIGURE 8-20 Schematic illustration of the accessory nerve, viewed from below.

Central connections of the hypoglossal nucleus include the corticobulbar (corticonuclear) motor system (with crossed fibers, as shown in Fig 7-9), as well as reflex neurons from the sensory nuclei of the trigeminal nerve and the nu- cleus of the solitary tract (not shown). Lesions of the medulla produce characteristic symptoms that are related to the involvement of the nuclei of the last four cranial nerves that lie within the medulla and the motor and sensory pathways through it. Extramedullary lesions of the posterior fossa may involve the roots of the last four cranial nerves between their emergence from the medulla and their exit from the skull.

TABLE 9-1 Functional Divisions of Thalamic Nuclei.

FIGURE 9-1 Midsagittal section through the diencephalon.

FIGURE 9-3 _ Diagrams of the thalamus. Oblique lateral and me- dial views.

FIGURE 9-5 Horizontal section through the thalamus.

hypothalamic nucleus; and the inferior mamillary peduncle, which sends fibers from the tegmentum of the midbrain. A small number of ganglion cells from throughout the retina (less than 1% of the total number of retinal ganglion cells) send axons that provide visual input to the suprachiasmatic nucleus via the retinohypothalamic tract. These and other connec- tions are shown in Table 9-2. Afferent connections to the hypothalamus include part of he medial forebrain bundle, which sends fibers to the hypo-

FIGURE 9-7 Coronal sections through the diencephalon and adjacent structures. A: Section through the optic chiasm and the anterior commissure. B: Section through the tuber cinereum and the anterior portion of the thalamus. C: Section through the mamillary bodies and middle thalamus. D: Key to the section levels.

FIGURE 9-8 The human hypothalamus, with a superimposed diagrammatic representation of the portal-hypophyseal vessels. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.)

* A, principally afferent; E, principally efferent. Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 76th ed. Appleton & Lange, 199 TABLE 9-2 Principal Pathways to and from the Hypothalamus.

FIGURE 9-9 Schematic view of the pituitary portal system of vessels and neurohypophyseal pathways. The portal hypophyseal ves- sels serve as a vascular conduit that carries various hypophyseotropic hormones from their sites of release from hypothalamic neurons, in the median eminence on the pituitary stalk, to the anterior pituitary. In contrast, the axons of supraoptic and paraventricular neurons run all the way to the posterior pituitary, where they release vasopressin and oxytocin.

FIGURE 9-11 Anterior pituitary hormones. ACTH, adrenocorticotropic hormone; TSH, thyroid-stimulating hormone; FSH, follicle- stimulating hormone; LH, luteinizing hormone; B-LPH, beta-lipotropin (function unknown). |1n women, FSH and LH act in sequence on the ovary to produce growth of the ovarian follicle, ovulation, and formation and maintenance of the corpus luteum. |n men, FSH and LH con- trol the functions of the testes. Prolactin stimulates lactation. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.) The epithalamus consists of the habenular trigones on each side of the third ventricle, the pineal body (pineal gland or epiphysis cerebri), and the habenular commissure (see Fig 9-1). The pineal body is a small mass that normally lies in the de- pression between the superior colliculi (Figs 9-1 and 9-13). Its base is attached by the pineal stalk. The ventral lamina of

FIGURE 9-10 Effects of hypophyseotropic hormones on the secretion of anterior pituitary hormones. CRH, corticotropin-releasing hormone; TRH, thyrotropin-releasing hormone; GnRH, gonadotropin-releasing hormone; GRH, growth hormone-releasing hormone; GIH, growth hormone-inhibiting hormone; PRH, prolactin-releasing hormone; PIH, prolactin-inhibiting hormone. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.)

TABLE 9-3 Principal Hypothalamic Regulatory Mechanisms.

FIGURE 9-12 Clock genes turn on and off, once per daily cycle, within neurons of the suprachiasmatic nucleus. Top panels show that transcription of the Per? gene peaks at about mid-day (Perl mRNA within suprachiasmatic neurons appears black). Bottom panels show Perl protein, which is produced after a delay of about 6 hours, peaking in the early evening. Per1 protein appears light. (Reproduced, with permission, from Mendoza J, Challet E: Neuroscientist 2009;5:480.) Reproduced and modified, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. Appleton & Lange, 2005.

FIGURE 9-13 Location of the circumventricular organs. There is no blood-brain barrier in these organs (see Chapter 11). CLINICAL CORRELATIONS Lesions in the subthalamic nucleus can result in hemiballis- mus, a motor disorder that affects one side of the body, causing coarse flailing of the arm or leg. (In rare cases, the lesions cause ballismus, affecting both sides.) Flailing of the affected extremities may lead to severe trauma or fractures. Lesions in the subthalamic nucleus can result in hemiballis-

FIGURE 10-1 Cross sections showing early development from neural groove to cerebrum.

FIGURE 10-2 Differential growth of the cerebral hemisphere and deeper telencephalic structures.

FIGURE 10-3 Coronal sections showing development of the basal ganglia in the floor of the lateral ventricle.

FIGURE 10-4 Dorsal view of developing cerebrum showing formation of the corpus callosum, which covers the subarachnoid cistern an vessels over the diencephalon.

E 10-5 Lateral view of the left cerebral hemisphere, showing principal gyri and sulci.

FIGURE 10-7 _ Dissection of the left hemisphere to show the insula.

FIGURE 10-8 Magnetic resonance image of a horizontal section through the upper head.

FIGURE 10-10 Diagram of the structure of the cerebral cortex. A: Golgi neuronal stain. B: Nissl cellular stain. C: Weigart myelin stain. D: Neuronal connections. Roman and Arabic numerals indicate the layers of the isocortex (neocortex); 4, external line of Baillarger (line of Ger nari in the occipital lobe); 5b, internal line of Baillarger. (A,B, and C reproduced, with permission, from Ranson SW, Clark SL: The Anatomy ofthe Nervous System, 10th ed. Saunders, 1959. D reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. Appleton & Lange, 2005.)

GURE 10-11 Lateral aspect of the cerebrum. The cortical areas are shown according to Brodmann with functional localizations.

-IGURE 10-12 Medial aspect of the cerebrum. The cortical areas are shown according to Brodmann with functional localizations.

FIGURE 10-13 Lateral view of the left hemisphere showing the functions of the cortical areas.

FIGURE 10-14 Motor homunculus drawn on a coronal section through the precentral gyrus. The location of cortical control of vari- ous body parts is shown.

FIGURE 10-15 Sensory homunculus drawn overlying a coro- nal section through the postcentral gyrus. The location of the cortical representation of various body parts is shown.

FIGURE 10-16 Magnetic resonance image showing Heschl’s gyrus (HG, red) and planum temporal (PT, blue) within the upper part of the temporal lobe. (Reproduced, with permission, from Oertel-Knéchel V, Linden DEJ: Neuroscientist 2011;17: 457.)

FIGURE 10-17 Motor activity in the cerebral cortex, visualized with functional magnetic resonance imaging. Changes in signal intensity, measured using a method called echoplanar magnetic res- onance imaging, result from changes in the flow, volume, and oxygenation of the blood. This study was performed on a 7-year-old boy. The stimulus was repetitive squeezing of a foam-rubber ball at the rate of two to four squeezes per second with the right or left hand. Changes in cortical activity associated with squeezing the ball with the right hand are shown in black. Changes in cortical activity associated with squeezing the ball with the left hand are shown in white. (Data from Novotny EJ, etal: Functional magnetic resonance imaging (fMRI) in pediatric epilepsy. Epilepsia 1994;35 (Supp 8):36.)

FIGURE 10-19 Spatial relationships between basal ganglia, thalamus, and internal capsule as viewed from the left side. Sections through planes A and B are shown in Figures 10-19A and B.

FIGURE 10-20 A: Frontal section through cerebral hemispheres showing basal ganglia and thalamus. B: Horizontal section through rearohral hamicnharac

FIGURE 10-22 Relationships between internal capsule, basal ganglia, and thalamus in horizontal section. Notice that descending motor fibers for the face, arm, and leg (F, A, L) run in front of ascend- ing sensory fibers (f, a, |) in the posterior limb of the internal capsule. (Modified from Simon RP, Aminoff MJ, Greenberg DA: Clinical Neurology, 4th ed. Appleton & Lange, 1999.)

FIGURE 10-21 Connections between the basal ganglia, the thalamus, and the cortex.

FIGURE 10-23 Magnetic resonance image of a horizontal section through the head.

FIGURE 10-24 Magnetic resonance image showing infarction in the posterior limb of the left internal capsule, which produced a “pure motor stroke” in an 83-year-old woman. The patient presented with acute onset of weakness of the right face, arm, and leg. (Courtesy of Joseph Schindler, M.D., Yale Medical School.)

FIGURE 11-2 Three stages of development of the choroid plexus in the lateral ventricle (coronal sections).

FIGURE 11-5 A: Schematic illustration of a coronal section through the brain and coverings. B: Enlargement of the area at the top of A.

FIGURE 11-3 _ Dorsal view of the choroid plexus in the ventric- ular system. Notice the absence of choroid in the aqueduct and the anterior and posterior horns.

The tentorium cerebelli separates the occipital lobes from the cerebellum. It is a roughly transverse, shelflike mem- brane that attaches at the rear and side to the skull at the trans- verse sinuses; at the front, it attaches to the petrous portion of the temporal bone and to the clinoid processes of the sphe- noid bone. Toward the midline, it fuses with the falx cerebri. The free, curved anterior border leaves a large opening, the

FIGURE 11-4 Drawing of the ventricles showing their relation- ship to the dura, tentorium, and skull base. One of the dural septa, the falx cerebri, extends like a curtain, down into the longitudinal fissure between the cere- bral hemispheres (Figs 11-5 and 11-6). It attaches to the inner surface of the skull in midplane, from the crista galli to the in- ternal occipital protuberance, where it becomes continuous with the tentorium cerebelli.

FIGURE 11-7 Schematic illustration of the brain showing spaces that contain CSF.

TABLE 11-1 Normal Cerebrospinal Fluid Findings.

FIGURE 11-10 = Schematic illustration, in coronal projection, of the circulation (arrows) of CSF.

FIGURE 11-13 Computed tomography image of a horizontal section through the head of a 7-year-old child with noncommunicat- ing hydrocephalus owing to the obstruction of the outflow foramens by a medulloblastoma.

FIGURE 11-14 Schematic illustration of the effect of obstruc- tion of reabsorption of CSF causing communicating hydrocephalus. Arrows indicate transependymal flow (compare with Figs 11-10 and

FIGURE 11-12 Hydrocephalus in a 14-month-old infant. FIGURE 11-11 Schematic illustration of the effects of obstruction of the cerebral aqueduct causing noncommunicating hydrocephalus. Arrows indicate transependymal flow (compare with Fig 11-10). Other possible sites of obstruction are the interventricular foramen and the outflow foramens of the fourth ventricle.

FIGURE 11-15 Schematic illustration of the relationships and the barriers between the brain, the meninges, and the vessels.

IGURE 11-16 Basal view of the skull, external aspect. Major bones are labeled in blue.

TABLE 11-3 Structures Passing Through Openings in the Cranial Floor.

FIGURE 11-17 | Floor of the cranial cavity, internal aspect.

FIGURE 11-18 Basal view of the skull, internal aspect. Major openings are highlighted in color.

FIGURE 11-19 An81-year-old woman was admitted with shortness of breath and fever. She was found to have a right middle lobe pneumonia, the third pneumonia in three months. Neurologic examination r evealed a vocal cord paralysis on the right side; the gag reflex was absent and there was loss of bulk of the trapezius and sternocleidomastoid muscles on the right side; the t ongue appeared slightly atrophic o1 the right and deviated to the right upon protrusion; there was asymmetric elevation of the soft palate (deviation to the left due to paralysis on the right side). The patient aspirated during a swallowing evaluation. Magnetic resonance imaging of the brain demonstrated amass lesion within the jugular foramen and the petrous bone on the right side [left image, arrow heads]. Computed t omography of the base of the skull showed osteolytic changes within the right petrous temporal and occipital bone [right: arrow heads; asterisk: jugular foramen]. A biopsy confirmed the clinically suspected diagnosis of glomus jugulare tumor which had impaired function of the ninth, t enth, eleventh and twelfth cranial nerves. The patient was treated with radiation. (Courtesy of Dr. Joachim Baehring.)

FIGURE 12-2 Circle of Willis and principal arteries of the brain stem.

FIGURE 12-3 Principal arteries on the floor of the cranial cavity (brain removed).

FIGURE 12-4 Arterial supply of the brain stem. A: Midbrain. The basilar artery gives off paramedian branches that supply the oculomotor (Ill) nerve nucleus and the red nucleus (RN). A larger branch, the posterior cerebral artery, courses laterally around the midbrain, giving off a basal branch that supplies the cerebral peduncle (CP) and a dorsolateral branch supplying the spinothalamic tract (ST), medial lemniscus (ML), and superior cerebellar peduncle. The posterior cerebral artery continues (upper arrows) to supply the thalamus, occipital lobe, and medial temporal lobe. B: Pons. Paramedian branches of the basilar artery supply the abducens (VI) nucleus and the medial lemniscus (ML). The anterior inferior cerebellar artery gives off a basal branch to the descending motor pathways in the basis pontis (BP) and a dorsolateral branch t 0 the trigeminal (V) nucleus, the vestibular (VIII) nucleus, and the spinothalamic tract (ST) before passing to the cerebellum (upper arrows). C: Medulla. Paramedian branches of the vertebral arteries supply descending motor pathways in the pyramid (P), the medial lemniscus (ML), and the hypoglossal (XII) nucleus. Another vertebral branch, the posterior inferior cerebellar artery, gives off a basal brancht o the olivary nuclei (ON) and a dorsolateral branch that supplies the trigeminal (V) nucleus, the vestibular (VIII) nucleus, and the spinothalamic tract (ST) on its way to the cerebellum (upper arrows). (Reproduced, with permission, from Simon RP, Aminoff MJ, Greenberg DA: Clinical Neurology, 4th ed. Appleton & Lange, 1999.)

FIGURE 12-5 Magnetic resonance image of a horizontal sec- tion at the level of the circle of Willis.

FIGURE 12-6 Arterial supply of the primary motor and sensory cortex (coronal view). Notice the location of the homunculus with respect to the territories of the cerebral arteries. (Reproduced, with permission, from Simon RP, Aminoff MJ, Greenberg DA: Clinical Neurology, 4th ed. Appleton & Lange, 1999.) Venous channels lined by mesothelium lie between the inner and outer layers of the dura; they are called intradural (or dural) sinuses. Their tributaries come mostly from the neigh- Cavernous sinuses: on either side of the sella turcica. The cavernous sinuses receive drainage from multiple sources, including the ophthalmic and facial veins. Blood leaves the cavernous sinuses via the petrosal sinuses (see Fig 12-8). The cavernous sinuses are convoluted, with different chambers separated by fibrous trabeculae; thus, they have the appearance of a cavern. A number of important arteries and cranial nerves are embedded with- in the cavernous sinus and its walls. The internal carotid

FIGURE 12-9 Three-dimensional view of veins and sinuses of the brain, left posterior lateral view.

Surrounding the area of infarction, there is often a penumbra, in which neurons have been metabolically com- promised and are electrically silent but are not yet dead. Neu- rons within the penumbra may be salvageable, and various

FIGURE 12-11 The cavernous sinus and associated structures. A: Relationship to skull and brain. B: The cavernous sinus wraps around the pituitary. Several important structures run through the cavernous sinus: the internal carotid artery; the oculomotor, trochlear, and abducen: nerves; and the ophthalmic branch of the trigeminal nerve and trigeminal ganglion.

TABLE 12-1 Clinical Profile of Cerebrovascular Disorders.

FIGURE 12-14 A. Computed tomography image of a horizon- tal section of the head showing an infarct caused by middle cerebral artery occlusion. B. Magnetic resonance image of horizontal section of the head from another patient who also sustained an infarct in the distribution of the left middle cerebral artery. This patient presented with sudden onset of aphasia and right-sided weakness. (Courtesy of Joseph Schindler, MD, Yale Medical School.)

FIGURE 12-13 Coronal section through the cerebrum show- ing a large infarct caused by occlusion of the internal carotid artery. The extent of an infarct depends on the presence or ab- sence of adequate anastomotic channels. The extent of the in- farct will often confirm to the territory supplied by the oc- cluded artery, as shown in Figure 14A, B. Capillaries from adjacent vascular territories and corticomeningeal capillaries at the surface may reduce the size of the infarct. When arterial occlusion occurs proximal to the circle of Willis, collateral

FIGURE 12-12 Schematic illustration of stages of occlusion of the internal carotid artery. (Modified and reproduced, with permission, from Poirer J, Gray F, Escourolle R: Manual of Basic Neuropathology. 3rd ed. WB Saunders, 1990.)

Data from Hass WK, Fields WS, North RR, Kiercheffll, Chase NE: Joint study of extracra nial arterial occlusion. JAMA 1968;203:961. TABLE 12-2 Frequency Distribution (in %) of Arterial Lesions Causing Cerebrovascular Insufficiency.

PIsVNe Fo bw VISTMOUTION OF GEGeENerdaliVe IESiONs IN lage cerebral arteries of the circle of Willis. The severity of the lesions is il- lustrated by the intensity of the shaded areas; the darkest areas show the most severe lesions. The principal pathologic change in the arteries of the brain oc- curs in the vasculature of the neck and brain, although similar changes may also be present in other systemic vessels. Distur- bances in metabolism, especially of fats, are believed to be a prominent associated change. Hypertension accelerates the progression of atherosclerosis and is a treatable risk factor for stroke.

Atheromatous changes in the arterial system are found rel- atively frequently at postmortem examination among those who have reached middle age (Fig 12-15). They are particularly com- mon in patients with untreated hypertension or with unfavor- able lipid profiles. Vessels of all sizes may be affected. A combi- nation of degenerative and proliferative changes can be seen microscopically. The muscularis is the main site of proliferation; the intima may be absent. The areas most often involved are near branchings or confluences of vessels (Fig 12-16 and Table 12-2). The most common and severe atherosclerotic lesions are in the carotid bifurcation. Others occur at the origin of the vertebral ar- teries, in the upper and lower parts of the basilar artery, and in the internal carotid artery at its trifurcation, the first third of the middle cerebral artery, and the first part of the posterior cerebral artery. Narrowing of vessels severe enough to cause vascular in- sufficiency is more frequent in older persons.

Modified with permission from Rowland LP: Clinical syndromes of the brain stem. IN Kandel ER, Schwartz JH (editors): Principles of Neural Science, 2nd edition. Elsevier, 198! TABLE 12-3 Brain Stem Syndromes Resulting from Vascular Occlusion.

FIGURE 12-18 (Continued) C: The patient was taken to angiography where he received stenting of the right vertebral artery as well as thrombolysis by selective intraarterial tPA (not shown). A follow up CT 24 hours after initial presentation demonstrated the ex- pected ischemic infarct in the cortical and subcortical substance of the left insular region and adjacent frontal and temporal lobes. The originally identified tissue at risk on CT-perfusion maps was salvaged (arrows). The patient's neurological status continued to improve after intervention and he was left with only mild right facial droop and mild right upper extremity pronator drift t wo days after initial pres- entation. (Courtesy of Nils Henninger, M.D.)

Congenital berry aneurysms are seen most frequently in the circle of Willis or in the middle cerebral trifurcation; they are especially common at sites of arterial branching. Aneurysms are seen infrequently in vessels of the posterior fossa. A ruptured aneurysm generally bleeds into the sub- arachnoid space or, less frequently, into the brain substance itself.

FIGURE 12-20 Hemorrhage in the right posterior thalamus and internal capsule in a 64-year-old woman.

FIGURE 12-21 Computed tomography image of a horizontal section through the head, showing high densities, representing a subarachnoid hemorrhage (arrows) in the sulci.

FIGURE 12-22 A: Computed tomography image of a horizontal section through the head, showing a large aneurysm of the anterio communicating artery. (Reproduced, with permission, from deGroot J: Correlative Neuroanatomy of Computed Tomography and Magnetic Resonance Imaging. Lea & Febiger, 1984.) B: Corresponding angiogram showing the partially thrombosed aneurysm (arrows).

FIGURE 12-23 Magnetic resonance image of a horizontal section through the head, demonstrating an arteriovenous malformation (arrows).

FIGURE 12-25 Schematic illustration of a subdural hamarrhanga

FIGURE 12-24 Magnetic resonance image of a horizontal sec- tion through the head, showing a left subdural hematoma (arrows) causing a midline shift.

FIGURE 12-26 Schematic illustration of an epidural hemorrhaae.

FIGURE 12-27 Computed tomography image of a horizontal section through the head, showing an extradural hematoma and in- tracerebral contrecoup lesion. (Reproduced, with permission, from deGroot J: Correlative Neuroanatomy of Computed Tomography and Magnetic Resonance Imaging. 21st ed. Appleton & Lange, 1991.)

FIGURE 13-1 Schematic illustration of some pathways control- ling motor functions. Arrows denote descending pathways.

FIGURE 13-2 A:Basal ganglia: major structures. MD, medial dorsal; VA, ventral anterior; VL, ventral lateral nuclei of thalamus. B: Majc afferents to basal ganglia. C: Intrinsic connections. D: Efferent connections.

TABLE 13-1 Summary of Reflexes. Another important feedback loop involves the second major outflow nucleus of the basal ganglia, the substantia ni- gra, which is reciprocally connected with the putamen and caudate nucleus. Dopaminergic neurons in the pars com- pacta of the substantia nigra project to the striatum (the ni- grostriatal projection), where they form inhibitory synapses on striatal neurons that have D2 dopamine receptors, and ex- citatory synapses on neurons that have D1 dopamine recep- tors (see Fig 13-2B). Reciprocal projections travel from the striatum to the substantia nigra (striatonigral projection) and are also inhibitory (see Fig 13-2C). This loop travels along the pathway The pars reticulata of the substantia nigra (SNr) receives input from the striatum, and sends axons outside the basal ganglia to modulate head and eye movements.

FIGURE 13-3 Diagram of the corticospinal tract, including de- scending fibers that provide sensory modulation to thalamus, dorsal column nuclei, and dorsal horn.

FIGURE 13-6 A: Conceptual model of activity in the basal ganglia and associated thalamocortical regions under normal circumstances. Dark arrows indicate inhibitory connections, and Open arrows indicate excitatory connections. B: Changes in activity in Parkinson's disease. As a result of degeneration of the pars compacta of the substantia nigra, differential changes occur in the two striatopallidal projections (as indicated by altered thickness of the arrows), including increased output from GPi to the thalamus. D, direct pathway; I, indirect pathway; GPe, external segment of globus pallidus; GPi, internal segment of globus pallidus; SNc, sub- stantia nigra (pars compacta); SNr, substantia nigra (pars reticulata); STN, subthalamic nucleus; VL, ventrolateral thalamus. (Reproduced with permission from Wichmann T, Vitek JL, DeLong MR: Parkinson's disease and the basal ganglia: Lessons from the laboratory and from neurosurgery, Neuroscientist 1995:1:236-244.)

TABLE 13-2 Signs of Various Lesions of the Human Motor System.

FIGURE 13-9 Midbrain of a 45-year-old woman with Parkinson's disease, showing depigmentation of the substantia nigra

FIGURE 13-8 Schematic illustration of the processes underly- ing Parkinsonism. GABA, gamma-aminobutyric acid. (Reproduced, with permission, from Katzung BG: Basic and Clinical Pharmacology, 9th ed. Appleton & Lange, 2004.)

IGURE 14-1 Schematic illustration of a spinal cord segment with its dorsal r oot, ganglion cells, and sensory organs.

TABLE 14-1 Differences between Lemniscal and Ventrolateral Systems.

FIGURE 14-2 Dorsal column system for discriminative touch and position sense (lemniscus system). FIGURE 14-3 Spinothalamic tracts for pain and temperature (ventrolateral system).

FIGURE 14-4 Major spinal pathways. The solid line on the right represents the line of incision in performing an anterolateral cordotomy. Notice the lamination of the tracts. S, sacral; L, lumbar; T, thoracic. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 16th ed. Apple ton & Lange, 1993.)

FIGURE 14-6 Diagram of convergence theory of referred pain. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.) After injury to a peripheral nerve or root, some of the in- jured axons may generate inappropriate repetitive impulses, which can result in chronic pain. This is especially common when, as a result of an unsuccessful attempt at regeneration,

FIGURE 14-5 Overview of the pain matrix. White arrows; as- cending and intracerebral pain pathways. Blue arrows; modulatory descending pathways. A, amygdale; ACC, anterior portion of cingu- late cortex; Cer, cerebellum; H, hypothalamus; |, insula; L, m lateral and medial thalamic nuclei; Mi, primary motor cortex; NA, nucleus accumbens; PAG, periaqueductal gray mattere; PFC, prefrontal cortex; PPC, posterior parietal cortex; $1, S2 primary and secondary somatosensory cortex; SMA, supplementary motor area. (Reproduced, with permission, from Borsook D, Sava S, Becerra L: The pain imaging revolution: ad- vancing pain into the 21st century Neuroscientist 2009;16:172.)

FIGURE 14-7 Schematic illustration of the pathways involved in pain control. (Courtesy of Al Basbaum.) A 41-year-old man was admitted to the hospital with pro- gressive weakness and unsteadiness of his legs. His dis- ability had begun more than a year earlier with tingling (“pins and needles”) feelings in his feet. Gradually, these sensations had become more disagreeable, and burning pains developed on the soles of his feet. The rest of his feet had become numb, and his legs had become weak. For about 6 months, he had had tingling feelings in his fingers and hands; his fingers felt clumsy, and he often dropped things. He had lost more than 6 kg (about 14 Ibs) during the previous 6 months. The patient had smoked about 30 cigarettes daily for many years and drank eight glasses of beer and half a bottle of whiskey (or more) each day. After losing his job a year before, the patient had worked at sev- eral unskilled jobs.

FIGURE 15-1 Horizontal section of the left eye; representation of the visual field at the level of the retina. The focus of the point of fixation is the fovea, the physiologic blind spot on the optic disk, the temporal (lateral) half of the visual field on the nasal side of the retina, and the nasal (medial) half of the visual field on the temporal side of the retina. (Reproduced, with permission, from Simon RP, Aminoff MJ, Greenberg DA: Clinical Neurology, 4th ed. Appleton & Lange, 1999.)

FIGURE 15-2 Section of the retina of a monkey. Light enters from the bottom and traverses the following layers: internal limiting membrane (ILM), ganglion cell layer (G), internal plexiform layer (IP), internal nuclear layer (IN) (bipolar neurons), external plexiform layer (EP), external nuclear layer (EN) (nuclei of rods and cones), external limiting membrane (ELM), inner segments of rods (IS) (narrow lines) and cones (triangular dark structures), outer segments of rods and cones (OS), retinal pigment epithelium (RP), and choroid (C). x655.

FIGURE 15-3 Neural components of the retina. C, cone; R, rod; MB, RB, FB, bipolar cells (of the midget, rod, and flat types, respectively); DG and MG, ganglion cells (of the diffuse and midget types, respectively); H, horizontal cells; A, amacrine cells. (Reproduced, with permission from Dowling JE, Boycott BB: Organization of the primate retina: Electron microscopy. ProcRoy Soc Lond Ser B [Biol] 1966;166:80.)

FIGURE 15-4 Schematic diagram of a rod and cone in the rotina

FIGURE 15-6 Thenormal fundus as seen through an ophthal- moscope. (Photo by Diane Beeston; Reproduced, with permission, from Riordan- Eva P, Whitcher JP: Vaughan & Asbury’s General Ophthalmology, 17th ed. McGraw-Hill, 2008.)

FIGURE 15-7 Accommodation. The solid lines represent the shape of the lens, iris, and ciliary body at rest, and the dotted lines represent the shape during accommodation. (Reproduced, with permis: sion, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.) When one views a distant object, the normal (emmetropic) eye is unaccommodated and the object is in focus. A normal eye readily focuses an image of a distant object on its retina, 24 mm behind the cornea; the focal length of the optics and the distance from cornea to retina are well matched, a state known as emmetropia (Fig 15-8). To bring closer objects into focus, the eye must increase its refractive power by accommo- dation. The ability of the lens to do so decreases with age as the lens loses its elasticity and hardens. The effect on vision usually becomes noticeable at approximately 40 years of age; by the 50s, accommodation is generally lost (presbyopia).

D. Refraction FIGURE 15-5 Probable sequence of events involved in photo- transduction in rods and cones. cGMP, cyclic guanosine monophos- Lo ee eS a ee ee a ee The lens is held in place by fibers between the lens capsule and the ciliary body (Figs 15-1 and 15-7). In the unaccommo-

FIGURE 15-10 Monocular and binocular visual fields. The dotted line encloses the visual field of the left eye; the solid line en- closes that of the right eye. The common area (heart-shaped clear zone in the center) is viewed with binocular vision. The shaded areas are viewed with monocular vision. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.) The visual pathways project from the retina, via the optic nerve, to the brain where they eventually reach the occipital cortex. Since the visual pathways extend over a long course, they are susceptible to injury at multiple points. An under- standing of the anatomy of the visual pathways is thus essential

FIGURE 15-8 Emmetropia (normal eye) and hyperopia and myopia (common defects of the eye). | n hyperopia, the eyeball is too short, and light rays come to a focus behind the retina. A biconvex lens corrects this by adding to the refractive power of the lens of the eye. In myopia, the eyeball is too long, and light rays focus in front of the retina. Placing a biconcave lens in front of the eye causes the light rays to diverge slightly before striking the eye, so that they are brought to a focus on the retina. (Reproduced, with permission, from Ganong WF: Review of Medica Physiology, 22nd ed. McGraw-Hill, 2005.)

Anatomy FIGURE 15-9 Visual field charts. Small white objects subtending 1° are moved slowly to chart fields on the perimeter. The smaller the object, the more sensitive the t est is (with a gross error of refraction, 1° is reliable). Red has the smallest normal field and gives the most sensitive field test. (Reproduced, with permission, from Riordan-Eva P, Whitcher JP: Vaughan & Asbury’s General Ophthalmology, 14th ed. McGraw-Hill, 1995.) Perimetry is used to determine the visual fields (Fig 15-9). The field for each eye (monocular field) is plotted with In assessing visual acuity, distant vision is tested with Snellen or similar cards for persons with fairly normal vision. Finger counting and finger movement tests are used for those with subnormal vision, and light perception and projection for those with markedly subnormal vision. Near vision is tested with standard reading cards.

FIGURE 15-11 Optic neuritis (papillitis) with disk changes, in- cluding capillary hemorrhages and minimal edema. (Compare with Fig 15-12.) (Reproduced with permission from Vaughan D, Asbury T, Riordan-Eva P: Vaughn & Asbury‘s General Ophthalmology, 14th edition, McGraw-Hill, 1995.)

FIGURE 15-12 Papilledema causing moderate disk elevation without hemorrhages. (Reproduced with permission from Vaughan D, Asbury T, Riordan-Eva P: Vaughn & Asbury’s General Ophthalmology, 14th edition, McGraw-Hill, 100c¢ \

FIGURE 15-13 Optic atrophy. Note avascular white disk anc avascular network in surrounding retina. (Reproduced with permission from Riordan-Eva P, Witches JP: Vaughn & Asbury’s General Ophthalmology, 17th edition, McGraw-Hill, 2008.)

FIGURE 15-14 The visual pathways. The solid blue lines represent nerve fibers that extend from the retina to the occipital cortex and carry afferent visual information from the right half of the visual field. The broken blue lines show the pathway from the left half of the visual fields. The black lines represent the efferent pathway for the pupillary light reflex.

FIGURE 15-15 Medial view of the right cerebral hemisphere showing projection of the retina on the calcarine cortex.

TABLE 15-1 Local Effects of Drugs on the Eye.

FIGURE 15-16 Typical lesions of the visual pathways. Their effects on the visual fields are shown on the right side of the illustration. A: Blindness in one eye. B: Bitemporal hemianopia. C: Homonymous hemianopia. D: Quadrantanopsia. E: Homonymous hemianopia.

FIGURE 15-18 Activation of visual cortex as shown by functional magnetic resonance imaging (fMRI). A: An oblique axial anatomic MRI. The region showing increased activity in response to a full-field patterned stimulus has been assessed by fMRI (using a method known as echoplanar MRI) and is shown in white. B: Activation of the visual cortex on the left side in response to patterned visual stimulation of the right visual hemifield (black) and activation of the right-sided visual cortex in response to patterned stimulation of the left hemifield. The changes in signal intensity are the result of changes in flow, volume, and oxygenation of the blood in response to the stimuli. (Data from Masuoka LK, Anderson AW, Gore JC, McCarthy G, Novotny EJ: Activation of visual cortex in occipital lobe epilepsy using functional magnetic r esonance imaging. Epilepsia 1994;35[Supp 8]:86.) “ As visual information is relayed from cell to cell in the primary visual cortex, it is processed in increasingly complex

FIGURE 15-17 Occipital hematoma (arrow) resulting from a bleeding arteriovenous malformation. This lesion produced homony- mous hemianopia and headache. (Reproduced, with permission, from Riordan-Eva P, Whitcher JP: General Ophthalmology, 17th ed. McGraw-Hill, 2008.)

FIGURE 15-20 Receptive fields of cells in visual pathways. Left: Ganglion cells, lateral geniculate cells, and cells in layer IV of cortical area 17 have circular fields with an excitatory center and an inhibitory surround or an inhibitory center and an excitatory surround. There is no pre- ferred orientation of a linear stimulus. Center: Simple cells respond best to a linear stimulus with a particular orientation in a specific part of the cell's receptive field. Right: Complex cells respond to linear stimuli with a particular orientation, but they are less selective in t erms of location in the receptive field. They often respond maximally when the stimulus is moved laterally, as indicated by the arrow. (Modified from Hubel DH: The visual field cortex of normal and deprived monkeys. Am Sci 1979;67:532. Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 19th ed. Appleton & Lange, 1999.) inance, and they are organized into another overlapping se- ries of ocular dominance columns, each 0.8 mm in diameter. The ocular dominance columns receiving input from one eye alternate with columns receiving input from the other (Fig 15-21). About one half of the complex cells in the visual cortex receive inputs from both eyes. The inputs are similar for the two eyes in terms of the preferred orientation and loca- tion of the stimulus, but there is usually a preference for one eye. These cells are referred to as showing ocular dom-

FIGURE 15-19 Light micrograph of the primary visual cortex (calcarine cortex) on each side of the calcarine fissure.

FIGURE 15-21 Reconstruction of ocular dominance columns in a subdivision of layer IV of a portion of the rightvisual cortex of a rhesus monkey. Dark stripes represent one eye; light stripes represent the other. (Reproduced, with permission, from LeVay S, Hubel DH, Wiesel TN: The pattern of ocular dominance columns in macaque visual cortex re- vealed by a reduced silver stain. J Comp Neurol 1975;159:559.)

FIGURE 16-1 Thehuman ear. The cochlea has been turned slightly, and the middle ear muscles have been omitted to make the relationship clear.

elicits a depolarization in peripheral branches of neurons of the cochlear ganglion. As a result, action potentials are pro- duced that are transmitted to the brain along axons that run within the cochlear nerve.

FIGURE 16-3 Cross section through one turn of the cochlea.

FIGURE 16-4 Structure of hair cell. (Reproduced with permission from Hudspeth AJ: The hair cells of the inner ear. They are exquisitely sensitive trans- ducers that in human beings mediate the senses of hearing and balance. A tiny force applied to the top of the cell produces an electrical signal at the bottom, Sci Am Jan;248(1):54-64, 1983.)

FIGURE 16-2 Schematic view of the ear. As sound waves hit the tympanic membrane, the position of the ossicles (which move as shown in blue and black) changes.

FIGURE 16-5 The vestibulocochlear nerve.

FIGURE 16-6 _ Diagram of main auditory pathways superimposed on a dorsal view of the brain stem.

FIGURE 16-7 Left: Middle ear, or conduction, deafness. Representative air conduction curve shows greatest impairment of pure t one thresholds in lower frequencies. Right: Perception, or nerve, deafness. Representative bone conduction curve of pure t one thresholds shows greatest deficit at higher frequencies.

and blinking with the right eye. Tests of air and bone

REFERENCES Allum JM, Allum- Mecklenburg Dj, Harris FP, Probst R (editors): 4 ‘nm

FIGURE 16-8 Magnetic resonance image of a horizontal sec- tion through the head at the level of the lower pons and internal au- ditory meatus. A left acoustic nerve schwannoma withits high inten- sity is shown in the left cerebellopontine angle ( arrow). ABLE 16-1 Common Tests with a Tuning Fork to Distinguish between Nerve and Conduction Hearing Loss.

FIGURE 17-1) Thehumanear (compare with Fig 16-1).

The kinetic labyrinth consists of the three semicircular canals. Each canal ends in an enlarged ampulla, which con- tains hair cells, within a receptor area called the crista am- pullaris. A gelatinous partition (cupula) covers each ampulla and is displaced by rotation of the head, displacing hair cells so that they generate impulses. The three semicircular canals are oriented at 90° to each other, providing a mechanism that is sensitive to rotation along any axis.

FIGURE 17-2 Principal vestibular pathways superimposed on a dorsal view of the brain stem. Cerebellum and cerebral cortex removed. (Reproduced, with permission, from Ganong WF: Review of Medical Phys- iology, 22nd ed. McGraw-Hill, 2005.)

FIGURE 17-3 Macular structure. (Reproduced, with permission, from Junqueira LC, Carneiro J, Kelley RO: Basic Histology, 11th ed. McGraw-Hill, 2005.)

FIGURE 17-4 Diagram of a crista in an opened ampulla.

FIGURE 17-5 Schematic illustration of the effects of head movements (top) and the subsequent cessation of movement (bottom) on the crista and the direction of endolymph flow. When the head moves, a compensatory adjustment of gaze, the vestibulo-ocular reflex, is required to keep the eyes fixed on one object. Clockwise rotation of the eyes is triggered by counterclockwise rotation of the head so as to maintain fix- ation of the eyes on a target in the external world. The path- ways for the reflex are via the medial longitudinal fasciculus and involve the vestibular system and the motor nuclei for eye movement within the brainstem (see Fig 8-7).

FIGURE 17-6 Example of caloric test with normal results. Stim- ulation of left ear for 40 s with cool (30 °C) water produces nystagmus lasting 110 seconds.

FIGURE 18-2 Lesions that cause coma or loss of consciousness.

Slightly modified and reproduced, with permission, from Rimel RN, Jane JA, Edlich RF: Injury scale for comprehensive management of CNS trauma. JACEP 1979;8.64.

FIGURE 18-3 | Sleep stages. Notice low muscle tone with extensive eye movement in rapid eye movement (REM) sleep. EOG, electro-ocu- logram registering eye movements; EMG, electromyogram registering skeletal muscle activity. Central, Frontal, and Occip indicate the three electroencephalographic leads. (Reproduced, with permission, from Kales A, Beall GN, Berger RJ et ak Sleep and dreams: Recent r esearch on clinical aspects. Ann Intern Med 1968;68:1078.)

TABLE 19-2 Major Limbic System Connections.

TABLE 19-1 Components of the Limbic System and Neocortex.

URE 19-1 = Schematic illustration of the location of the limbic system between the diencephalon and the neocortical hemispheres.

FIGURE 19-2 = Schematic illustration of the concentric main components of the limbic sytem. The dentate gyrus is one of the few regions of the mam- malian brain where neurogenesis (the production of new neu- rons) continues through adulthood.

FIGURE 19-6 Neural elements in the olfactory bulb. and constitutes the major outflow pathway from the hip- pocampus. Its fibers start as the alveus, a white layer on the ventricular surface of the hippocampus that contains fibers from the dentate gyrus and hippocampus (see Figs 19-8 and 19-10). From the alveus, fibers lead to the medial aspect of the hippocampus and form the fimbria of the fornix, a flat band of white fibers that ascends below the splenium of the corpus callosum and bends forward to course above the thal- amus, forming the crus (or beginning of the body) of the fornix. The hippocampal commissure, or commissure of the

FIGURE 19-5 The olfactory nerves (lateral view).

FIGURE 19-9 = Schematic illustration of a coronal section showing the components of the hippocampal formation and subicu- lum. (Compare with Fig 19-8.) CA, through CA, are sectors of the hippocampus. Much of the hippocampal input is relayed via the en- torhinal cortexfrom the temporal neocortex.

FIGURE 19-7 Olfactory connections projected on the basal aspect of the brain (intermediate olfactory tract not labeled).

-IGURE 19-8 = Micrograph of a coronal section through the medial temporal lobe.

to reach the parahippocampal gyrus (see Fig 19-11). Thus, t he following circuit is formed: This circuit, called the Papez circuit after the neu- roanatomist who defined it, ties together the cerebral cortex and the hypothalamus. It provides an anatomic substrate for the convergence of cognitive (cortical) activities, emotional experience, and expression.

parahippocampal gyrus > hippocampus —> fornix mamillary bodies — anterior thalamic nuclei > cingulate gyrus > parahip- pocampal gyrus

FIGURE 19-12 _ Diagram of the principal connections of the limbic system. A: Hippocampal system and great limbic lobe. B: Olfactory and amygdaloid connections.

FIGURE 19-13 Location of the amygdale (red) within a coro- nal slice of the brain. (Reproduced, with permission, from Koenigs M, Grafman J: Neuroscientist 2009;15:54 1.)

FIGURE 19-14 Horizontal section through the head at the level of the midbrain and amygdala. (Reproduced, with permission, from deGroot J: Correlative Neuroanatomy of Computed Tomography and Magnetic Reso- nance Imaging. 21st ed. Appleton & Lange, 1991.)

FIGURE 19-15 Magnetic resonance image of horizontal sec- tion through the head at the level of the temporal lobe. The large lesion in the left temporal lobe and a smaller one on the right side are indicated by arrowheads. Computed tomography scans confirmed the presence of multiple small hemorrhagic lesions in both temporal lobes.

FIGURE 20-1 Overview of the sympathetic nervous system and of its sympathetic (thoracolumbar) and parasympathetic (craniosacral divisions. Inf., inferior; Sup., superior.

FIGURE 20-2 Sympathetic division of the autonomic nervous system (left half). CG, celiac ganglion; IMG, inferior mesenteric ganglio: SMG, superior mesenteric ganglion.

FIGURE 20-3 Types of outflow in autonomic nervous system. Pre, preganglionic neuron; Post, postganglionic neuron; CR, communicat- ing ramus. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. McGraw-Hill, 2005.)

JRE 20-5 Parasympathetic division of the autonomic nervous system (only left half shown).

TABLE 20-1 Pain Innervation of the Viscera.

FIGURE 20-7 Sympathetic pathways to the eye and orbit. Interruption of these pathways inactivates the dilator muscle and thereby produces miosis, inactivates the tarsal muscle and produces the effect of enophthalmos, and reduces sweat secretion in the face (Horner’s syndrome).

FIGURE 20-6 Horner's syndrome in the right eye, associated with a tumor in the superior sulcus of the right lung.

FIGURE 20-8 Location of carotid and aortic bodies. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 22nd ed. Appleton & Lange, 2005.)

FIGURE 20-9 _ Descending pathway and innervation of the uri- nary bladder.

FIGURE 20-11 Flaccid neurogenic bladder, caused by a lesion of either the sacral portion of the spinal cord or the cauda equina.

FIGURE 20-10 Spastic neurogenic bladder, caused by a more or less complete transection of the spinal cord above S2.

TABLE 20-2 Responses of Effector Organs to Autonomic Nerve Impulses and Circulating Catecholamines.

*Depends on stage of menstrual cycle, amount of circulating estrogen and progesterone, pregnancy, and other factors. tOn palms of hands and in some other locations (adrenergic sweating). EN ne EE I ee Se Se Te ee ee eT ey I, Le Ta Le a a NS ee ee eee CT eee eee | hee TABLE 20-2 Responses of Effector Organs to Autonomic Nerve Impulses and Circulating Catecholamines. (Cont.)

FIGURE 20-12 = Schematic diagram showing some anatomic and pharmacologic features of autonomic and somatic motor nerves. ACh, acetylcholine; NE, norepinephrine. The target tissues on which norepinephrine acts can be sepa- rated into two categories, based on their different sensitivities to certain drugs. This is related to the existence of two types

FIGURE 20-13 Preganglionic and postganglionic receptors at the endings of a noradrenergic neuron. The preganglionic receptor shown is a; the postganglionic receptors can be 044, 02, B,, or Bz. NE, norepinephrine. (Reproduced, with permission, from Ganong WF: Review of Med- ical Physiology, 18th ed. Appleton & Lange, 1997.)

* Not available in the USA. t Note that guanethidine is believed to have two principal actions. + Clonidine stimulates 0.2 receptors in the periphery, but along with other 02 agonists that cross the blood-brain barrier, it also stimulates 02 receptors in the brain, which crease sympathetic output. Therefore, the overall effect is decreased sympathetic discharge. Modified and reproduced, with permission, from Ganong WF: Review of Medical Physiology, 18th ed. Appleton & Lange, 1997.

FIGURE 21-1 Central speech areas of the dominant cerebral hemisphere. Notice that Broca’s and Wernicke’s areas are interconnected via fibers that travel in the arcuate fasciculus, subja- cent to the cortex.

FIGURE 21-2 Magnetic resonance images of sections through the head. Top: Horizontal section with a large high-intensity area in the temporal lobe, representing an infarct caused by occlusion of a middle cerebral artery branch. Bottom: Coronal section showing the same area of infarction. (Parallel lines on the periphery of the brain represent artifacts caused by patient motion.) Large infarcts of this type, in the dominant cerebral hemisphere, can produce global aphasia that is accompanied by hemiparesis.

-IGURE 21-3 Neuroanatomic basis for the syndrome of alexia without agraphia. Damage to two regions (the visual cortex in the left, peech-dominant hemisphere and the splenium of the corpus callosum, which carries interhemispheric al xons connecting the t wo visual ortices) is required. These regions are both irrigated by the posterior cerebral artery. Thus, occlusion of the left posterior cerebral artery can roduce this striking syndrome.

FIGURE 21-4 Magnetic resonance image showing lesions in the left occipital lobe and splenium ofthe corpus callosum in a 48-year-old man who suddenly developed a right superior visual field of quadrantanopsia and alexia without agraphia. Both hyperten- sion and hypercholesterolemia placed this patient at high risk for stroke.

FIGURE 21-5 Unilateral (left-sided) neglect in a patient with a right hemispheric lesion. The patient was asked to fill in the numbers on the face of a clock (A) and to draw a flower (B).

FIGURE 21-6 Magnetic resonance image showing infarction in the territory ofthe right middle cerebral artery, in a history professor who presented with weakness on the left side and left-sided neglect. A contralateral neglect syndrome is often seen with right hemispheric lesions. The patient was not aware of his left-sided weakness, and failed to respond to stimuli on his left side. (Courtesy of Dr.Joseph Schindler, Yale Medical School.)

FIGURE 21-7 Brain areas concerned with encoding long-term memories. (Reproduced, with permission, from Ganong WF: Review of Medical Physiology, 19th ed. Appleton & Lange, 1999.)

This 44-year-old woman had a generalized tonic— clonic seizure associated with fever at the age of 3 but was otherwise well until the age of 12, when complex partial seizure activity began. Her seizures were characterized by an aura consisting of a rising sensation in her gut, followed by loss of conscious- ness, tonic activity of the left hand, and turning of the head to the left. Sometimes she would fall if standing. Her seizures av- eraged 5 to 10 per month despite treatment with anticonvul- sant drugs. On examination, no neurologic abnormalities were observed. Because of the failure of traditional medical therapy to control her seizures, the patient was hospitalized. Elec- troencephalogram monitoring revealed slowing and abnor- mal spike activity in the right anterior temporal lobe. During her seizures there was abnormal discharge of the right tempo- ral lobe. An intracarotid amobarbital test, in which an anes- thetic was injected into her carotid arteries, demonstrated left-hemisphere dominance for speech and a marked disparity of memory function between the left and right hemispheres; the left hemisphere showed perfect memory and the right showed significantly impaired memory. Magnetic resonance

FIGURE 21-9 Magnetic resonance image of frontal section through the head, showing hippocampal atrophy (arrow) in the patient described in Clinical Illustration 21-1.

FIGURE 21-10 Postoperative magnetic resonance image of frontal section through the head, showing anteromedial temporal lobectomy (arrow).

FIGURE 22-1 Planes used in modern imaging procedures.

FIGURE 22-2 Angiogram of the aortic arch and stem vessels. Normal image. 1: Brachiocephalic artery; 2: common carotid artery; 3: left subclavian artery; 4: right vertebral artery. (Reproduced, with per- mission, from Peele TL: The Neuroanatomical Basis for Clinical Neurology. Blakiston, 1954.)

FIGURE 22-4 Schematic drawing of a normal angiogram of the internal carotid artery, arterial phase, lateral projection. The num- bers refer to vessels shown in Figures 22-4 and 22-6. (Redrawn and re- produced, with permission, from List C, Burge M, Hodges L: Intracranial angiogra- phy. Radiology 1945;45:1.)

FIGURE 22-5 Left internal carotid angiogram, arterial phase, lateral view. Normal image (compare with Fig 22-6).

FIGURE 22-7 Right internal carotid angiogram, arterial phase, anteroposterior view. Abnormal image.

FIGURE 22-8 Vertebral angiogram, arterial phase, right lateral view. Normal image. Arrows indicate posterior choroidal arteries.

The CT scanning apparatus rotates a narrow x-ray beam around the head. The quantity of x-ray absorbed in small vol- umes (voxels [volume elements, or units]) of brain, measuring approximately 0.5 mm? x 1.5 mm or more in length, is com- puted. The amount of x-ray absorbed in any slice of the head can be thus determined and depicted in various ways as pixels

FIGURE 22-9 Vertebral angiogram, arterial phase, anteropos- terior view, with head flexed (Towne position). An aneurysm is pres- ent, but the pattern of the vessels is normal.

jURE 22-10 Left internal carotid angiogram, venous phase, lateral view. Normal image. (Compare with Figs 12-9 and 22-11.)

FIGURE 22-12 Digital subtraction angiogram of the neck ves- sels, oblique anterior view. Open arrow shows small sclerotic plaque; closed arrow shows large plaque.

FIGURE 22-13 Schematic image of the zero horizontal and coronal planes. The line between anterior and posterior commissures parallels Reid’s base plane.

FIGURE 22-11 Schematic drawing of normal venogram in lateral projection, obtained by carotid injection. Superficial veins are shadec more darkly than the sinuses and deep veins. (Redrawn and reproduced, with permission, from List C, Burge M, Hodges L: Intracranial angiography. Radiology 1945;45:1.)

FIGURE 22-15 CTimage, with contrast enhancement, of a horizontal section at the level of the thalamus. Normal image. Com- pare with Figure 13-5.

FIGURE 22-14 Lateral “scout view” used in CT procedure. Su- perimposed lines represent the levels of the images (sections). Line 1 is at the level of the foramen magnum line 4 is at the level of the in- fraorbitomeatal plane.

Brain tumor. Cerebellar medullo- blastoma in a 16-year-old male. Brain tumor. Cerebral metastasis from carcinoma of lung in a 65- year-old man.

FIGURE 22-17 Schematic representation of MR imager and its components. (Reproduced with permission from deGroot J: Correlative neuroanatomy of computed tomography and magnetic resonance imaging, 21st edition. Appleton & Lange, 1991.)

FIGURE 22-21 Example of functional MRI showing increased perfusion of the motor cortex in the right hemisphere associated with rapid finger tapping of the left hand. Upper left: Relative blood flow map in the transverse (horizontal) plane during rest. Upper right: Relative blood flow map during rapid tapping of fingers of the left hand (the arrows point to the region in the right hemisphere where the increased blood flow response is seen). Lower right: Subtracting one image from the other provides a “difference image,’ which shows a hot spot corre- sponding to the active region of the cortex. Center: Difference image superimposed on structural MRI, showing that increased perfusion maps precisely to the motor cortex in the anterior bank of the central sulcus of the right hemisphere. (Courtesy of Dr. S. Warach.) Positron emission tomography (PET) scanning has become a major clinical research tool for the imaging of cerebral blood low, brain metabolism, and other chemical processes (Fig 22-22). Radioisotopes are prepared in a cyclotron and are inhaled or injected. Emissions are measured with a gamma-ray

POSITRON EMISSION TOMOGRAPHY of the fingers), sensory activity (ie, stimulation of a sensory organ or part of the body surface), cognitive activity (eg, cal- culation, reading, or recalling), and affective activity (eg, responding mentally to a fearful stimulus). Examples are shown in Figures 15-17 and 22-21.

FIGURE 22-23 SPECT image of a horizontal section through the head at the level of the temporal lobe. An infarct (arrow) is shown as an interruption of the cortical ribbon. (Courtesy of D. Price.)

FIGURE 22-22 PéTscan of a horizontal section at the level of the lateral ventricles. The various shades of gray indicate different levels of glucose utilization.

FIGURE 23-1 Asingle-plane projection of the head, showing all standard positions of electrode placement and the locations of the central sulcus (fissure of Rolando) and the lateral cerebral fissure (fissure of Sylvius). The outer circle is drawn at the level of the nasion and inion; the inner circle represents the temporal line of electrodes. This diagram provides a useful guide for electrode placement in rou- tine recording. A, ear; C, central; Cz, central at zero, or midline; F, frontal; Fp, frontal pole; Fz, frontal at zero, or midline; O, occipital; P, parietal; Pg, nasopharyngeal; Pz, parietal at zero, or midline; T, temporal. (Courtesy of Grass Technologies, An Astro Med, Inc. Produce Group, West Warwick, RI.)

:pilepsy. EEG of a 6-year-old child who had suffered three major convulsions, two which appeared to start in theleft extremities. -IGURE 23-2 Representative electroencephalograms.

FIGURE 23-3 Far-field recording of brain stem auditory response latencies in humans showing proposed functional-anatomic correlations. Diagram shows normal latencies for vertex-positive brain stem auditory evoked potentials (waves I-IV) evoked by clicks of 60 dBHL (60 dB above normal hearing threshold) at a rate of 10/s. Lesions at different levels of the auditory pathway t end to produce response abnormalities beginning with the indicated components. Intermediate latency (5.8 ms) between latencies of waves IV and V is the mean peak latency of fused wave IV/V when present. C,,, vertex positivity, represented by an upward pen deflection; C,_, vertex negativity, represented by a downward pen deflection. (Reproduced, with permission, from Stockard JJ, Stockard JE, Sharbrough FW: Detection and localization of occult lesions with brain stem auditory responses. Mayo Clin Proc 1977;52:761.)

FIGURE 23-4 Action potentials in electromyography. A: Nerve potential from normal muscle; B: fibrillation potential and C: positive wave from denervated muscle; D: high-frequency discharge in myotonia; E: bizarre high-frequency discharge; F: fasciculation potential, single discharge; G: fasciculation potential, repetitive or grouped discharge; H: synchronized repetitive discharge in muscle cramp; I: diphasic, J: triphasic, and K: polyphasic motor unit action potentials from normal muscle; L: short-duration motor unit action potentials in progressive mus: cular dystrophy; M: large motor unit action potentials in progressive muscular dystrophy; N: highly polyphasic motor unit action potential and short-duration motor unit action potential during reinnervation. Calibration scale (vertical) in microvolts. The horizontal scale shows 1000-Hz waveforms. An upward deflection indicates a change of potential in the negative direction at the needle electrode. (Reproduced, with permission, from Clinical Examinations in Neurology, 3rd ed. Members of the Section of Neurology and Section of Physiology, Mayo Clinic and Mayo Foundation f or Medical Education and Research, Graduate School, University of Minnesota, Rochester, MN. WB Saunders, 1971.)

TABLE 24-1 Characteristic Cerebrospinal Fluid Profiles.

FIGURE 25-2 Magnetic resonance image (surface coil technique) of a parasagittal section through the lumbar spine in a patient with a root tumor (arrow).

FIGURE 25-3 Ventral view of the spinal cord (with the dura opened) of a patient with motor neuron disease (amyotrophic lateral sclerosis). Notice the reduction in size of the ventral roots (resulting from the degeneration of the axons of motor neurons) compared with the normal dorsal roots.

FIGURE 25-5 Photograph ofa horizontal section through L4-5 intervertebral disk in a patient withlow back pain. Note the lat- eral herniation of the nucleus pulposus. (Reproduced, with permission, from deGroot J: Correlative Neuroanatomy of Computed Tomography and Magnetic Resonance Imaging. Lea & Febiger, 21st ed. Appleton & Lange, 1991.)

FIGURE 25-4 Magnetic resonance image (surface coil technique) of a sagittal section through the lower lumbar spine of a patient with low back pain. Note the herniation of the nucleus pulpo- sus at L4—5 compressing the cauda equina.

TABLE 25-1 Frequency of Major Types of Intracranial Tumors. * Exclusive of pituitary tumors. Reproduced, with permission, from Way LW (editor): Current Surgical Diagnosis & Treat- ment, 70th ed. Appleton & Lange, 1994.

FIGURE 25-8 Magnetic resonance image of a horizontal sec- tion through the head of a 28-year-old patient showing the lesions (arrowheads) of multiple sclerosis.

FIGURE 25-6 Photograph of a section through the open medulla (from Wallenberg’s original publication). A large infarct is vis- ible on the right and a smaller one on the left ( arrows).

FIGURE 25-7 Left posterior inferior cerebellar artery occlusion (Wallenberg’s syndrome).

FIGURE 25-12 Magnetic resonance image of a horizontal sec tion through the head at the level of the lentiform nucleus in a patient with a glioma surrounded by edema (arrows).

FIGURE 25-11 Coronal section through the brain of a patient with a hemispheric glial tumor. Histopathologic examination showed this to be a glioblastoma. Note the uncal and subfalcial herniations (arrowheads). A biopsy track is visible on the left (arrow),

FIGURE 25-10 Magnetic resonance image through the base of the brain in a patient with a pituitary adenoma (arrow). The tumor has grown downward into the sphenoid sinus and upward to the optic chiasm.

Reproduced, with permission, from Dunphy JE, Way LW (editors): Current Surgical Diagnosis & Treatment, 3rd ed. Appleton & Lange, 1977 TABLE 25-2 Brain Tumor Types According to Age and Site.

FIGURE 25-14 Computed tomography image of a horizontal section through the temporal lobes, showing an epidural lesion and multiple rounded confluent masses in the right lobe.

FIGURE 25-13 Computed tomography image of a horizontal section through the head at the level of the lateral ventricles in a pa- tient with glioblastoma multiforme. A small amount of blood lies in the bottom ofa cystic portion ofthe tumor.

FIGURE 25-18 Computed tomography image through the head at the level of the external ears (bone window) in a patient with epidural hemorrhage. Note the fracture site (arrow) and nearby air bubbles. Neurosurgical treatment of the bleeding and prompt re- moval of the epidural blood may be lifesaving.

FIGURE 25-25 Computed tomography image, with contrast enhancement, of a horizontal section through the cerebral hemispheres. The absence of surrounding edema suggests a slow- growing tumor, in this case a meningioma.

FIGURE 25-23 Distribution of sensory and lower-motor- neuron deficits in a patient with peripheral polyneuropathy. Notice the “stocking-and-glove" pattern of sensory loss.

FIGURE 25-24 Olfactory groove meningioma. (From Scarf: PIQGUNRE 49-49% Olfactory groove meningioma. (From Scarff: Classic Syndromes of Brain Tumor. Annual Clinical Conference of the Chicago Medical Society, 1953.)

First stage: Tinnitus; later, deafness and disturbances of equilibrium.

FIGURE 25-28 Computed tomography image, with contrast enhancement, of a horizontal section through the head. Notice the low-density cystic astrocytoma with a high-density nodule in the posterior fossa, representing a glioma of the cerebellum. The history indicates a series of transient ischemic attacks, which are suggestive of cerebrovascular occlusive disease. The most common cause in elderly persons is arteriosclerosis. The sudden deterioration of the patient’s status was caused by thrombotic or embolic occlusion of a major cerebral vessel on the right side. Papilledema indicated an intracranial mass ef- fect caused by swelling of the brain associated with an ischemic infarct. The flaccid paralysis and the sensory deficits suggested involvement of the blood supply to the sensory motor cortex or the underlying white matter in the right hemisphere. The

FIGURE 25-29 Magnetic resonance image of a midsagittal section through the head. The large mass that originates in the clivus and displaces the brain stem backward is a chordoma (arrows).

Comment: The most common posterior fossa tumors in children are astrocytomas, medulloblastomas, and ependy- momas. Different types of tumors may occur in older persons (Table 25-2 and Figs 25-27 to 25-29).

FIGURE 25-31 Computed tomography image of a horizontal section through the upper hemispheres of a patient with a known bronchial carcinoma.

FIGURE 25-30 Left internal carotid angiogram, arterial phase, lateral view, showing occlusion of the middle cerebral artery (arrow). The posterior artery is well filled (compare with Fig 22-4).

TABLE B-1_ Grading Muscle Strength. Modified from Aids to the Investigation of Peripheral Nerve Inquiries. Her Majesty's Royal Stationary Office. London, UK, 1953.

Modified and reproduced, with permission, from McKinley JC. TABLE B-2 (Continued).

FIGURE B-1 Trapezius, upper portion (C3, 4; spinal accessory nerve). The shoulder is elevated against resistance.

FIGURE B-2 Trapezius, lower portion (C3, 4; spinal accessory nerve). The shoulder is thrust backward against resistance.

FIGURE B-5 Infraspinatus (C4-6; suprascapular nerve). With the elbow flexed at the side, the arm is externally rotated against re- sistance on the forearm.

FIGURE B-6 Supraspinatus (C4-6; suprascapular nerve). The arm is abducted from the side of the body against r esistance.

FIGURE B-3 Rhomboids (C4, 5; dorsal scapular nerve). The shoulder is thrust backward against resistance.

FIGURE B-4 Serratus anterior (C5-7; long thoracic nerve). The patient pushes hard with outstretched arms; the inner edge of the scapula remains against the thoracic wall. (If the trapezius is weak, the inner edge may move from the chest wall.)

FIGURE B-9 Pectoralis major, upper portion (C5-8; T1; latera and medial pectoral nerves). The arm is adducted from an elevatec or horizontal and forward position against resistance.

FIGURE B-8 _ Deltoid (C5, 6; axillary nerve). Abduction of later- ally raised arm (30-75° from body) against resistance.

FIGURE B-10 Pectoralis major, lower portion (C5-8;T1; lateral and medial pectoral nerves). The arm is adducted from a forward po- sition below the horizontal level against resistance.

FIGURE B-7 _Latissimus dorsi (C5-8; subscapular nerve). The arm is adducted from a horizontal and lateral position against r esist- ance.

FIGURE B-14 Extensor digitorum (C7, 8; radial nerve). The fin- gers are extended at the metacarpophalangeal joints against resist- ance.

FIGURE B-11 Biceps (C5, 6; musculocutaneous nerve). The supinated forearm is flexed against resistance.

FIGURE B-13 _ Brachioradialis (C5, 6; radial nerve). The forearm is flexed against resistance while in a neutral position (neither pronated nor supinated). FIGURE B-12 Triceps (C6-8; radial nerve). The forearm, flexed at the elbow, is extended against resistance.

FIGURE B-15 Supinator (C5-7; radial nerve). The hand is supinated against resistance, with arms extended at the side. Resis- tance is applied by the grip of the examiner's hand on the patient's forearm near the wrist.

FIGURE B-17 Extensor carpi ulnaris (C6-8; radial nerve). The wrist joint is extended to the ulnar side against resistance. FIGURE B-16 Extensor carpi radialis (C6-8; radial nerve). The wrist is extended to the radial side against resistance; fingers remain extended.

FIGURE B-20 Extensor indicis proprius (C6-8; radial nerve). The index finger is extended against resistance placed on the dorsal aspect of the finger.

FIGURE B-21 Abductor pollicis longus (C7, 8; 11; radial nerve). The thumb is abducted against resistance in a plane at a right angle to the palmar surface.

FIGURE B-19 Extensor pollicis brevis (C7, 8; radial nerve). The thumb is extended at the metacarpophalangeal joint against resist- ance.

FIGURE B-23 Flexor digitorum superficialis (C7, 8;T1; median nerve). The fingers are flexed at the first interphalangeal joint against resistance; proximal phalanges remain fixed.

FIGURE B-22 Flexor carpi radialis (C6, 7; median nerve). The wrist is flexed to the radial side against resistance.

FIGURE B-18 Extensor pollicis longus (C7, 8; radial nerve). The thumb is extended against resistance.

FIGURE B-29 Opponens pollicis (C8, T1; median nerve). The thumb is crossed over the palm against resistance to touch the top of the little finger, with the thumbnail held parallel to the palm.

FIGURE B-24 Flexor digitorum profundus (C7, 8;T1; median nerve). The terminal phalanges of the index and middle fingers are flexed against resistance while the second phalanges are held in ex- tension.

FIGURE B-28 Flexor pollicis brevis (C7, 8; T1; median nerve) The proximal phalanx of the thumb is flexed against resistance placed on its palmar surface. FIGURE B-27 Flexor pollicis longus (C7, 8; T1; median nerve). The terminal phalanx of the thumb is flexed against resistance as the proximal phalanx is held in extension.

FIGURE B-26 Abductor pollicis brevis (C7, 8; T1; median nerve). The thumb is abducted against resistance in a plane at a right angle to the palmar surface. FIGURE B-25 Pronator teres (C6, 7; median nerve). The extended arm is pronated against resistance. Resistance is applied by the grip of the examiner's hand on the patient's forearm near the wrist.

FIGURE B-33 Opponens digiti quinti (C7, 8; T1; ulnar nerve). With fingers extended, the little finger is moved across the palm to the base of the thumb.

FIGURE B-31 Flexor carpi ulnaris (C7, 8; T1; ulnar nerve). The little finger is abducted strongly against resistance as the supinated hand lies with fingers extended on the table. FIGURE B-30 _Lumbricales-interossei, radial half (C8, T1; median and ulnar nerves). The second and third phalanges are extended against resistance; the first phalanx is in full extension. The ulnar has the same innervation and can be tested in the same man- ner.

FIGURE B-32 Abductor digiti quinti (C8,T1; ulnar nerve). The little finger is abducted against resistance as the supinated hand with fingers extended lies on the table.

FIGURE B-34 Adductor pollicis (C8, T1; ulnar nerve). A piece of paper grasped between the palm and the thumb is held against r e- sistance with the thumbnail kept at a right angle to the palm.

FIGURE B-35 Dorsal interossei (C8, T1; ulnar nerve). The index and ring fingers are abducted from the midline against resistance as the palm of the hand lies flat on the table.

FIGURE B-37 Sartorius (L2, 3; femoral nerve). With the patient sitting and the knee flexed, the thigh is rotated outward against re- sistance on the leg.

FIGURE B-47 Flexor hallucis longus (L5; $1, 2; tibial nerve). The great toe is plantar-flexed against resistance. The second and third toes are also flexed.

FIGURE B-46 Flexor digitorum longus (S1, 2; tibial nerve). The toe joints are plantar-flexed against resistance.

FIGURE B-50 Tibialis anterior (L4, 5; deep peroneal nerve). The foot is dorsiflexed and inverted against resistance applied by gripping the foot with the examiner's hand.

FIGURE B-48 Extensor hallucis longus (L4, 5; $1; deep peroneal nerve). The large toe is dorsiflexed against resistance.

FIGURE B-49 Extensor digitorum longus (L4, 5; 1; deep per- oneal nerve). The toes are dorsiflexed against resistance.

FIGURE B-52 Tibialis posterior (L5, 51; tibial nerve). The plantar-flexed foot is inverted against resistance applied by gripping the foot with the examiner's hand.

FIGURE B-51 Peroneus longus and brevis (L5, S1; superficial peroneal nerve). The foot is everted against resistance applied by gripping the foot with the examiner's hand.

FIGURE C-1 Motor and sensory levels of the spinal cord.

-IGURE C-4 Segmental innervation of the right upper extremity, anterior view.

FIGURE C-5 Segmental innervation of the right upper extremity, posterior view.

FIGURE C-6 Musculocutaneous (C5, 6) and axillary (C5, 6) nerves.

FIGURE C-11 The femoral (L2-4) and obturator (L2-4) nerves.

FIGURE C-13 Segmental innervation of the right lower extremity, anterior view. Note the similarity between dermatomes (on left) and myotomes (on right).

FIGURE C-14 Segmental innervation of the right lower extremity, posterior view.

FIGURE C-15 The sciatic nerve (L4, 5; $1-3).

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