Posted on. Page Count. Features Include: Clinical Connection boxes Review questions at the end of each chapter and detailed answers in the back of the book An entire chapter on locating lesions An atlas of myelin-stained sections Unique, hand-drawn, full color artwork A glossary of key terms. It seems that you're in Germany. We have a dedicated site for Germany. Editors: Cohen , Ronald A. Particularly significant developments in cognition and behavior research are coming from neuroimaging, a vital source of new studies on the role of the brain in health behavior.
Brain Imaging in Behavioral Medicine and Clinical Neuroscience presents in depth the latest clinical and research applications of neuroimaging, surveying frequently used methods among them fMRI, MRS, perfusion and diffusion imaging and their uses in understanding brain behavior and pathology.
Your email address will not be published. Basic Clinical Neuroanatomy by Paul A. File Name: basic clinical neuroscience free pdf. New Book — Memorable Neurology! Vascular accidents involving the vessels here result in subarachnoid hemorrhage.
The ependymal cells line the fluid-filled cavities or ventricles of the brain and the central canal of the spinal cord. The microglial cells are phagocytes that arise from macrophages and engulf the debris resulting from injury, infections, or diseases in the CNS. The macroglia consist of four cell types: Figure Relation of neurons, glia, and capillaries.
Each astrocyte has a star-shaped cell body and numerous irregularly shaped processes, some of which may be extremely long. Processes of some astrocytes have end-feet on the surface of the brain or spinal cord.
These end-feet form a protective covering called the external limiting membrane or glial membrane. Many astrocytic processes have vascular end-feet, which surround capillaries. The endothelial cells of CNS capillaries are interconnected by tight junctions and form the blood-brain barrier, which selectively governs the passage of materials, including many drugs, from the circulating blood into the CNS.
Astrocytes have other functions as well. Astrocytes are the first cells to undergo alterations in response to CNS insults such as ischemia, trauma, or radiation. Also, astrocytes form scars resulting from CNS injury. Astrocytes are highly susceptible to the formation of neoplasms.
Oligodendrocytes The formation and maintenance of CNS myelin are the primary functions of the oligodendrocytes, small glial cells with relatively few processes Fig. The myelin sheath is formed by oligodendrocyte processes, which wrap around the axon to form a tight spiral. The myelin itself is located within the processes. Each oligodendrocyte envelops a variable number of axons depending on the thickness of the myelin sheaths.
In the case of thin myelin sheaths, one oligodendrocyte may be related to 40 or 50 axons. Oligodendrocytes may also surround the cell bodies of neurons, but in this location they do not contain myelin. Recent research suggests that oligodendrocytes also produce neurotrophic factors, the most important of which is a nerve growth factor that may promote the growth of damaged CNS axons.
During development of the myelin sheath, the Schwann cell first encircles and then spirals around the axon many times, forming multiple layers or lamellae. The myelin is actually located within the Schwann cell lamellae Fig. The outermost layer of the Schwann cell lamellae is called the neurolemma or sheath of Schwann. Because each Schwann cell myelinates only a small extent of the axon, myelination of the entire axon requires a long string of Schwann cells.
Between each Schwann cell, the myelin is interrupted. These areas of myelin sheath interruption are called nodes of Ranvier Figs. Similar interruptions of myelin sheaths occur in the CNS. In unmyelinated fibers, one Schwann cell envelops many axons. Schwann cells not only form and maintain the myelin sheath but also are extremely important in the regeneration of damaged axons.
When an axon is cut, the part of the axon separated from the cell body degenerates; however, the string of Schwann cells distal to the injury proliferates and forms a tube.
Growth sprouts arising from the proximal end of the transected axon enter this tube and travel to the structures supplied by the axon before its injury. Such functional axonal regeneration is common in the PNS. Axonal regeneration has not occurred in the human CNS, and this lack of regeneration may be related, in part, to the absence of Schwann cells.
Unlike the oligodendrocyte, which envelops many myelinated axons, the Schwann cell envelops only part of one myelinated axon. Capsular Cells Capsular cells are the glial elements that surround the neuronal cell bodies in sensory and autonomic ganglia. The sensory ganglia of the spinal nerves Figure Myelinated axon in the peripheral nervous system.
Transverse view. Longitudinal view. Although capsular cells are present in autonomic ganglia, because of the irregular shapes of these ganglion cells the capsules are less uniform and, hence, incomplete. The cell body is the metabolic center of a neuron and contains the nucleus and the cytoplasm. The nucleus contains nucleoplasm, chro- matin, a prominent nucleolus and, in the female only, a nucleolar satellite.
The cytoplasm contains the usual cellular organelles such as mitochondria, Golgi apparatus, and lysosomes. In addition, various-sized clumps of rough endoplasmic reticulum, called Nissl bodies, are prominent in the cytoplasm of neurons.
However, the neuronal cytoplasm where the axon emerges is devoid of Nissl bodies; this area is called the axon hillock. Another cytoplasmic characteristic of neurons are neurofibrils, which are arranged longitudinally in the cell body, the axons, and dendrites. Neurons are classified morphologically as unipolar, bipolar, or multipolar according to their number of protoplasmic processes Fig.
The single process of a unipolar neuron is the axon. Unipolar neurons are located almost exclusively in the ganglia of spinal nerves and some cranial nerves. Bipolar neurons have an axon and one Anatomic axon physiologic dendrite Figure Morphologic types of neurons arrows indicate direction of impulses. All the remaining nerve cells are multipolar neurons and have an axon and between 2 and 12 or more dendrites.
Axons do not contain Nissl bodies, vary in length from microns to meters, and convey impulses away from the cell body. The integrity of the axon, regardless of its length, is maintained by the cell body via two types of axoplasmic flow or axonal transport. In anterograde axonal transport, the cell body nutrients are carried in a forward direction from the cell body to the distal end or termination of the axon.
Anterograde axonal transport is vital for axonal growth during development, for maintenance of axonal structure, and for the synthesis and release of neurotransmitters, the chemicals that assist in the transfer of nerve impulses from one cell to another. Besides anterograde transport, retrograde axonal transport occurs from the distal end of the axon back to the cell body.
The function of retrograde axonal transport is the return of used or worn out materials to the cell body for restoration. Myelinated axons are insulated by a sheath of myelin that starts near the cell body and stops just before the axon terminates Fig. Myelin is a multilayered phospholipid located within axonal supporting cells. The myelin sheath increases the conduction velocity of the nerve impulse along the axon.
The thicker the myelin sheath, the faster the conduction velocity. The junction between the axonal ending and the neuron, muscle cell, or gland cell is called the synapse.
An important anatomic characteristic of the synapse is that the axonal ending is separated from the surface of the other nerve, muscle, or gland cell by a space, the synaptic cleft.
An important physiologic characteristic of a synapse is polarization; that is, the impulse always travels from the axon to the next neuron in the circuit or to the muscle or gland cells supplied by the axon.
When a nerve impulse arrives at the synapse, chemicals called neurotransmitters are released into the synaptic cleft. Neurotransmitters, manufactured and released by the neurons, cross the synaptic cleft to affect the postsynaptic neuron, muscle, or gland cell. The transmitters at neuromuscular and neuroglandular synapses are excitatory; that is, they elicit muscle contraction or glandular secretion.
However, the neurotransmitters at synapses between neurons may be excitatory, enhancing the production of an impulse in the postsynaptic neuron, or inhibitory, hindering impulse production in the postsynaptic neuron.
This resting membrane potential results from the differential distribution of ions and selective membrane permeability with four major cations and anions contributing to the resting membrane potential.
Proteins and amino acids do not move through the membrane as part of the resting membrane potential. Electrotonic Conductance in the Soma-Dendritic Membrane Electrotonic transients in the resting membrane potential can result in the interior of the cell becoming relatively more negative or hyperpolarized or less negative or depolarized.
These potential shifts are electrotonically summated, temporally and spatially, as they are conducted passively from the soma and dendrites to the axon hillock-initial segment Fig. Action Potential Initiation and Conductance Depolarization of the axon hillock-initial segment region to about —45 mV results in the generation of an action potential.
Unlike in the soma and dendrites where membrane transients are graded, membrane conductance at the axon hillock-initial segment becomes self-sustaining with the initia- tion of an action potential. Starting at the initial axon segment and continuing through to its terminal branches the propagation of the action potential occurs as a nondecremental voltage change. The velocity of propagation of an action potential is dependent on axonal diameter and myelination.
Saltatory Conduction In unmyelinated, generally small-diameter 0. Action Potential Frequency Encodes Information Information is transmitted between neurons or between neurons and effector structures by the propagation of action potentials. In many neurons action potential frequency is linearly correlated with stimulus intensity and the resultant degree of depolarization of the soma-dendritic membrane.
The more sustained the depolarization, the greater the frequency of action potentials. Synaptic interactions: A. Excitatory postsynaptic potentials EPSPs can spatially summate when they converge as they are electrotonically conducted from the dendrites to the soma. EPSPs can summate temporally when the same synaptic input is activated rapidly by multiple presynaptic action potentials. Excitatory and inhibitory inputs are integrated at the initial segment and sufficient depolarization generates an action potential.
Synaptic Transmission The synapse is the point of functional contact between neurons, and the neuromuscular junction is the point of functional contact between axons and skeletal muscle.
Most synapses are electrochemical and mediated by neurotransmitters. Some synapses are characterized as fast when the delay between presynaptic release and postsynaptic action is about 0. Transmembrane changes mediated by inotropic receptors that quickly depolarize the postsynaptic neuron generate excitatory postsynaptic potentials EPSPs , whereas ionic changes that hyperpolarize the neuron are classified as inhibitory postsynaptic potentials IPSPs.
In the CNS, synaptic contacts can also be formed at en passant axonal swellings along axons. Acquired autoimmune disorders affect transmission at the neuromuscular junction. Myasthenia gravis is an autoimmune disease affecting nicotinic acetylcholine receptors, leading to skeletal muscle weakness and fatigability in orbital, oropharyngeal, and limb musculature.
Muscle weakness and fatigability is generally variable in severity and progressive through active hours of the day. Nerve fibers are intact, and acetylcholine release at the nerve terminal is normal. Antibodies attack the acetylcholine receptor in the postjunctional folds, leading to a progressive decrement in amplitude of the evoked end-plate potentials and decreased muscle action potentials with repetitive stimulation. Structural changes of the postjunctional folds and diminished localization of the receptor at the crest of the folds also occur.
Increasing the efficacy of the action of acetylcholine in the neuromuscular cleft with acetylcholinesterase inhibitors decreases the severity of the symptoms. Muscle weakness and fatigability is predominantly in proximal limb and trunk musculature as seen in Lambert-Eaton myasthenic syndrome owing to diminished presynaptic release of acetylcholine from the nerve terminals. Muscle excitability remains normal. Multiple focal areas of demyelination of spinal roots and proximal nerve fibers result in very slow nerve conduction velocities and reduced compound action potential amplitude in electrophysiologic recordings from affected nerves.
Symmetric and temporally progressive weakness in movements, first in the legs and then in the arms, gives the impression of an ascending 13 paralysis. Difficulties in walking and rising from a chair are common complaints. Paralysis of respiratory muscles results in a high risk of respiratory failure.
After treatment, functional recovery is possible by axonal remyelination. Charcot-Marie-Tooth disease type 1A is the most common hereditary polyneuropathy resulting in demyelination of sensory and motor axons.
Multiple sclerosis is the most common acquired demyelinating disease in the CNS with an immunologic cause. Symptomatology is dependent on the axonal tracts involved. Adjoining segments of myelin are lost demyelinating plaques in the white matter fiber tracts in the cerebrum, cerebellum, brainstem, and spinal cord. Normal impulse conduction occurs proximal and distal to the plaques but is blocked or slowed at the plaques. Biophysical properties of the demyelinated axolemma are altered, thereby affecting impulse propagation.
Multiple sclerosis is characterized by chronically protracted cycles of relapse and remission. Remission with improvement of symptoms reflects partial remyelination of the affected axonal segments.
Persistent deficits can reflect the failure to remyelinate or, more probably, axonal injury within the plaque and axonal degeneration. As a result, the loss of neurons is irreparable; a neuron once destroyed can never be replaced. Conversely, axons can regenerate and regain their functions even after being completely transected or cut, as long as the cell body remains viable. This capacity to regenerate is limited, however, to axons in the PNS.
Functional axonal regeneration has not occurred in the human CNS. Thus, the degeneration of neuronal cell bodies anywhere in the nervous system and the degeneration of CNS axons are irreparable. What are the two main classes of cells in the CNS? What is a synapse and what are the chief characteristics of synapses in the CNS? What is the significance of axoplasmic transport? What are the chief differences between astrocytes and oligodendrocytes?
Between which cranial structures are the following located? A common route whereby viruses such as polio or rabies travel to CNS neuronal cell bodies is via: a. The cell most commonly associated with CNS tumors is the: a.
Some , Americans must use wheelchairs because of spinal cord injuries. Most of these injuries result from trauma such as occurs in automobile or sports accidents. An estimated two-thirds of the victims are 30 years of age or younger; the majority are men.
T he spinal cord connects with the spinal nerves and is the structure through which the brain communicates with all parts of the body below the head. Impulses for the general sensations such as touch and pain that arise in the limbs, neck, and trunk must pass through the spinal cord to reach the brain, where they are perceived. Likewise, commands for voluntary movements in the limbs, trunk, and neck originate in the brain and must pass through the spinal cord to reach the spinal nerves that innervate the appropriate muscles.
Thus, damage to the spinal cord may result in the loss of general sensations and the paralysis of voluntary movements in parts of the body supplied by spinal nerves.
The spinal cord extends from the foramen magnum, the large opening in the base of the skull, to the first lumbar vertebra Fig. Superiorly, the spinal cord is continuous with the brain and, inferiorly, it ends by tapering abruptly into the conus medullaris Fig. However, high-velocity objects e. The cervical vertebrae are the smallest and most fragile and, hence, most fractures occur here.
The segments are named and numbered according to the attachment of the spinal nerves. The spinal nerves are named and numbered according to their emergence from the vertebral canal.
Spinal nerves C1 through C7 emerge through the intervertebral foramina above their respective vertebrae. The remaining spinal nerves emerge below their respective vertebrae Fig. Until the third month of fetal development, the position of each segment of the developing spinal cord corresponds to the position of each developing vertebra.
After this time, the vertebral column elongates more rapidly than the spinal cord. At birth, the spinal cord ends at the disc between LV2 and LV3. Further growth of the vertebral column results in the inferior or caudal end of the spinal cord being located in adulthood usually at the middle third of LV1.
However, variations from the middle third of TV11 to the middle third of LV3 may occur. The approximate relation between spinal levels and vertebral levels is shown in Figure The level of spinal cord lesions is always localized according to the spinal cord segment. Most spinal cord levels do not, however, correspond to vertebral levels. If neurosurgical procedures are to be performed, the spinal cord level must be correlated with the appropriate vertebral level.
From internal to external, the spinal meninges are called the pia mater, arachnoid, and dura mater Fig. The arachnoid loosely surrounds the spinal cord and is attached to the inner surface of the dura mater. The spinal cord is anchored to the Denticulate ligament Figure Relations of spinal meninges.
The denticulate ligaments are 21 pairs of fibrous sheaths located at the sides of the spinal cord. Medially, the ligaments form a continuous longitudinal attachment to the pia mater. Laterally, they form triangular, toothlike processes that attach to the dura. Because of their pial attachments midway between the posterior and anterior surfaces of the spinal cord, the denticulate ligaments can be used as landmarks for surgical procedures. The spinal cord is also anchored by the roots of the spinal nerves, which are ensheathed by a cuff of dura where they perforate it near the intervertebral foramina.
The area between the spinal dura and the periosteum lining the vertebral canal is the epidural space. Its contents include loose connective tissue, fat, and the internal vertebral venous plexus. It, therefore, provides a direct path for the spread of infections, emboli, or cancer cells from the viscera to the brain. Inferior or caudal to the spinal cord, the dura mater forms the dural sac Fig.
Caudal to this point, it surrounds the filum terminale, the threadlike extension of the pia mater, and descends to the back of the coccyx as the coccygeal ligament, which blends with the periosteum. Because the arachnoid is attached to the inner surface of the dura lining the dural sac, the contents of the sac are in the subarachnoid space. Therefore, the dural sac contains a the filum terminale; b the cauda equina, consisting of the lumbosacral nerve roots descending from the spinal cord to their points of emergence at the lumbar intervertebral and sacral foramina; and c cerebrospinal fluid.
The spinal cord ends just above LV2, whereas the subarachnoid space continues caudally to SV2. A hypodermic needle may be introduced into the subarachnoid space Fig. It is inadvisable to puncture above the LV2—3 interspace in adults and above the LV4—5 interspace in infants or small children. Thus, each segment gives rise to four separate roots, one posterior and one anterior on each side. Each of these individual roots is attached to the spinal cord by a series of rootlets. The posterior and anterior roots take a lateral and descending course within the subarachnoid space Fig.
The posterior root or spinal ganglia, groups of neurons in the posterior root, are within the thoracic, lumbar, and sacral intervertebral foramina but slightly distal to the cervical foramina.
The posterior and anterior roots unite immediately beyond the ganglia to form the spinal nerves, which then exit from the intervertebral foramina and immediately begin to branch.
The most prominent Figure Transverse section showing a composite of the structures in various spinal cord segments and the formation of a spinal nerve.
On the opposite side is a far less conspicuous groove, the posterior median sulcus. The anterior and posterior rootlets of the spinal nerves arise somewhat lateral to these median grooves, at the anterolateral and posterolateral sulci, respectively. The small posterior spinal arteries are located in the latter sulci.
The external part is the white matter, which consists of millions of axons transmitting impulses superiorly or inferiorly. A large number of the fibers are myelinated, thus accounting for the white color in the fresh or unstained state.
The internal part is the gray matter, which consists of nerve cell bodies and the neuropil that includes the dendrites, preterminal and terminal axons, capillaries, and glia between the neurons.
It contains some entering and exiting myelinated fibers but has a grayish color in the fresh or unstained state because of the virtual absence of myelin. According to their positions, these are the posterior funiculus, the lateral funiculus, and the anterior funiculus Fig. Each funiculus is subdivided into groups of fibers called fasciculi or tracts. As an example, at cervical levels each posterior funiculus is divided into a medial part, the gracile tract, and a lateral part, the cuneate tract.
A well-defined separation between these two tracts is not always evident. This is generally true of most of the tracts in the spinal cord; hence, the locations of the various tracts in the spinal white matter are based on postmortem studies of human subjects with known neurologic abnormalities.
The posterior or dorsal horns; 2. The anterior or ventral horns; 3. The intermediate zones; 4. The lateral horns. For descriptive purposes, an imaginary horizontal line passing from side to side through the deepest part of each posterior funiculus and extending laterally through the gray matter defines the anterior boundary of the posterior horns Fig.
The posterior horns contain groups of neurons that are influenced mainly by impulses entering the spinal cord via the posterior roots.
The anterior horns are located between the anterior and lateral funiculi. Most of their neurons play roles in voluntary movement and many of them give rise to axons that emerge in the anterior roots. The intermediate zones are located between the anterior and posterior horns and are continuous medially with the gray matter that crosses the midline at the central canal.
The intermediate zones are composed mainly of association or interneurons for segmental and intersegmental integration of spinal cord functions.
The lateral horn is a small triangular extension of the intermediate zone into the lateral funiculus of the thoracic and the upper two lumbar segments. It contains cell bodies of preganglionic neurons of the sympathetic nervous system. Nuclei or Cell Columns The neurons of the spinal gray matter are arranged in longitudinal groups of functionally similar cells referred to as columns or nuclei Fig.
Some of these nuclei extend through the entire length of the spinal cord, whereas others are found only at certain levels. Laminae The spinal gray matter can also be divided into laminae or layers based on layerings of morphologically similar neurons Fig.
Laminae provide a more precise identification of areas within the spinal gray matter and are very useful in describing the locations of the origins or terminations of the functional paths.
Ten laminae make up the spinal gray matter and, in general, they are numbered from posterior to anterior. Lamina X is in the commissural area surrounding the central canal. Because of the large size of the lower limbs, the lumbar and sacral segments have massive posterior and anterior horns. In lumbar segments, the anterior horn has a distinct medial extension, whereas in sacral segments the anterior horn extends laterally.
In addition, the rim of white matter surrounding the sacral gray matter is much thinner than that in the lumbar spinal cord. The posterior horn in both thoracic and cervical segments is narrow compared with lumbar and sacral segments. However, owing to the muscular volume of the upper limbs, the cervical anterior horn is much larger than the thoracic, which mainly supplies the relatively small intercostal and subcostal muscles. The thoracic segments have the least amount of gray matter, both anteriorly and posteriorly.
Differences in the amount of white matter are subtle throughout the spinal cord. Search Ebook here:. Designed by readallbooks. Download here Download Now here.
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