Last updated: 13th November 2007
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 This web site contains introductory remarks and notes relating toHuman Neuroanatomy lectures by J.A.Kiernan.

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The University of Western Ontario
Department of Anatomy and Cell Biology

Anatomy 530a.  Lecture notes.

Anatomy & Cell Biology 350a was a half-course appropriate to the third-year of an honours programme in biological or biomedical sciences. Owing to current limitations in laboratory and other facilities the course was largely restricted to students in the Occupational Therapy (OT) and Physical Therapy (PT) programmes. Every year a few graduate students took Anatomy & Cell Biology 530a, which was 350a with an additional assignment and exam.  These notes for 530a are more extensive and more detailed than the ones that were provided for Anatomy 350a. They remain on the Web  in the hope that they may be helpful to students learning  human neuroanatomy.

This document contains some advice to students that may no longer be relevant, because in 2007 Anatomy 350a and 530a  were replaced by a new integrated neurosciences course for OT and PT students at UWO. This is  531a Neuroscience for rehabilitation sciences, which is coordinated by  Dr D. Belliveau.

 Anatomy 535b  is a  graduate level course in neuroanatomy for research-oriented MSc or PhD students at UWO.

J. A. Kiernan  MB, ChB, PhD, DSc 
Professor, Department of Anatomy & Cell Biology
Room 453, Medical Sciences Building, U.W.O.

(ACB web page)  


Please read this.  It includes answers to many frequently asked questions.

If you have questions about the subject matter of this course, you are always welcome to ask them at any reasonable time.  My office is Room 453, Medical Sciences Building. You do not need to make an appointment. Call 661-2111 ext 86822 if you want to check that I'm there or ask a question on the phone. If you attend in person you will get better service. Talking on the phone is helpful only for highly specific questions that have short answers. You may also ask for very brief answers to questions by email: kiernan[AT]
Please come and see me as soon as you have difficulty understanding a topic.  Do not wait until the week immediately before an exam!

Instructional resources.    Ask Mr Michael Wu of the Department of Anatomy and Cell Biology (Room 440) if you wish to study in the Anatomy Museum on the 4th floor (Dent. Sci. Bldg. Room 4002). Our museum contains many neuroanatomy specimens and models. 
      For the lab classes you will need a CD-ROM, specially prepared for use in conjunction with this course by Mr Michael Wu. Unfortunately there is a charge of $5 to cover the cost of production of the CD-ROM.
      Dr D. G. Montemurro, formerly of the Department of Anatomy at UWO, has produced numerous VHS videotapes that explain the anatomy of the nervous system as it is seen in practical classes. Some will be shown in 350a classes. All are available in the Taylor Library.  Several of these tapes include more details than are needed for Anatomy 350a. The required level of detail is that presented in the lectures and shown on the CD-ROM.
      For students who like such things, two sets of interactive  Sample exam questions are available for downloading. There is also a sample of the video lab exam that will show you what to expect in the practical part of the mid-term tests.
      You can also download a glossary of neuroanatomical terms.

Instant neuroanatomy (BasicNeuro.pdf).    For an illustrated summary of the subject, click here. The file BasicNeuro.pdf can be read on screen or printed. (Use an inkjet printer if possible; most of the illustrations are in colour.)
(You need the free Adobe Acrobat Reader to read or print PDF files. If you don't have this program, click on the link to download it from

       If you understand everything in BasicNeuro.pdf and are familiar with the contents of the lab CD-ROM, you will certainly obtain at least a B grade for the course.

The plan.    The first two lectures introduce the major parts of the adult nervous system and explain how they develop in the embryo. Two lectures on the peripheral nervous system follow.
      The next five weeks are devoted to the anatomy of the central nervous system. There are one-hour lectures, but the anatomy is studied principally by examination of whole and dissected specimens of human brains in the Wednesday lab classes.
      The mid-term test has two parts: multiple choice questions based on the lectures, and a video practical exam based on the lab classes.  Note!  It is not possible to separate the lecture material completely from the lab material because many structures and functions are covered in both types of class.
      For a sample of the type of questions in the video practical exam, click here to download the file SampleVP.exe. Run the file (needs Windows 95 or later) to see a sample "lab" exam with five questions.
      The remainder of the course consists of lectures on systemic or functional neuroanatomy. For these, the teachers assume that the students remember most of the topographical neuroanatomy from the first half of the course. Not all the functional systems of the brain are included in this course. The last lecture brings together the pathways and the topographical neuroanatomy by showing that localized damage at different sites can produce a wide variety of functional deficits. Much of the material in this last lecture will be revision.
      The final examination will cover the whole subject, but most of the questions will related to material covered in the second half of the course. Questions in both exams will be set by the people who give the corresponding lectures.

The topics listed below correspond to the lecture titles. Click on a  link ,  below, for notes on the topic. Within each topic there are clickable links that show text notes, diagrams, downloadable files etc.  Use your web browser's "back" button to return from a link to this page.
Asterisks (***) indicate lectures by Dr W. Rushlow, who provides paper handouts. These links are not active in this version of the web notes for Anatomy 350a. (They are available, however, for graduate students taking the course as 530a.)

Introduction. Major parts of nervous system
Development of the nervous system Peripheral nervous system
Autonomic functions and neurotransmitters Anatomy of the spinal cord
The cerebral cortex Brain stem anatomy
Brain stem anatomy Internal anatomy of cerebrum and diencephalon
Arteries of the central nervous system Somatic sensory pathways
Descending motor pathways Cerebellum
Basal ganglia Cranial nerves I, II & VIII. Their central connections
Cranial nerves III, IV and VI Cranial nerves V, VII, IX, X, XI, XII
The hypothalamus and pituitary gland Prefrontal cortex and temporal lobes
Language and memory Cerebral artery occlusions
Brain stem strokes

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Introduction to Anatomy 350/530. Major parts of the central and peripheral nervous systems.

Now for the neuroanatomy!  Let's get started. 

The CNS.

The central nervous system (CNS) is a tube, closed at both ends. The thickness of the wall of the tube varies, being greatest at the rostral (cranial) end. The complicated shape of the brain is due partly to the need to fold it up to fit into the skull. The CNS is made of fragile, gelatinous tissue. It is contained entirely within the axial skeleton (cranium and vertebral column).

These are the major divisions of the CNS:
In this list the most commonly used names are in bold type.
   Spinal cord.
         [Cavity: central canal]
   Rhombencephalon or hindbrain
      (consisting of medulla, pons and
         [Cavities: central canal & 4th ventricle]
         [No internal cavity but near 4th ventricle]
   Mesencephalon or midbrain.
         [Cavity: cerebral aqueduct]
   Prosencephalon or forebrain (consisting of the
      diencephalon, and the telencephalon
         [Cavity: 3rd ventricle]
      or cerebral hemispheres, each of these divisions
      being composed of many smaller parts.
         [Cavities: lateral ventricles]

Nerves connect the CNS with all other parts of the body. A nerve is ensheathed in collagenous connective tissue and can withstand the changes in pressure and tension associated with moving jointed limbs. Nerves go out from the axial skeleton by way of foramina [foramen = hole] in the cranium (cranial nerves) and between vertebrae (spinal nerves). This general plan applies to all vertebrate animals - even ones that don't have limbs or bony skeletons.  
Generalized vertebrate nervous system
(Small plan of the nervous system)    (Big picture of the whole human nervous system)
Whole nervous system

Strategy for coping with terminology.

The greatest difficulty confronting the beginning student of neuroanatomy is becoming familiar with a large number of names of parts. Use the index or the glossary of your textbook to look up each new word you encounter. Do not attempt to learn the definition unless the word either
   (a) applies to structure associated with a function that you have been told about. An example is the calcarine sulcus, associated with vision.
   (b) is something conspicuous enough to be a landmark relating to the positions of other structures. For example, the lateral sulcus is near to areas of the cerebral cortex concerned with hearing, understanding what's heard, formulation of speech, the sense of taste, and other parts of the forebrain with known functions and connections.

The PNS.

The peripheral nervous system (PNS) is composed of nerves and ganglia. A ganglion is a collection of neuronal cell bodies outside the CNS. Typically a ganglion is a lump on a nerve, but many of the ganglia associated with internal organs are of microscopic size.


The cells that do the rapid communicating in the nervous system are neurons. These vary greatly in form (Picture of some types of neuron), but most types have long cytoplasmic extensions: dendrites typically conduct towards the cell body, and the single axon typically carries signals away from the cell body. The primary sensory neuron (dorsal root ganglion cell) differs from this typical form in being unipolar; the single process is an axon, and it conducts both towards and away from the cell body. Neurons

Grey matter, synapses and white matter.

Grey matter contains cell bodies of neurons in the CNS. It is pink because it contains many capillary blood vessels. It goes grey when the tissue is preserved in formaldehyde. Grey matter also contains dendrites and axons. Synapses are functional connections between neurons, typically from end branches of axons to dendrites. Synapses occur in grey matter (and also in autonomic ganglia).
(Diagram of some different sorts of synapse) Synapses

Myelin and nerve fibres.

Long axons in the CNS have myelin sheaths, formed from concentric layers of surface membrane derived from the ensheathing glial cells (oligodendrocytes). Conduction of signals occurs much more rapidly in a myelinated axon than in one that lacks a myelin sheath. Tissue consisting largely of myelinated axons in the CNS is called white matter; it is pale in fresh and in fixed tissue. In the PNS myelin sheaths are formed by the Schwann cells.
Myelin sheath formation in a peripheral nerve
A nerve fibre is an axon together with its myelin sheath.
An unmyelinated fibre is an axon that has no myelin sheath and therefore conducts slowly.


Other types of cell are also present in nervous tissue, and in the CNS these cells outnumber the neurons by 10:1. These are the neuroglial cells. In the PNS satellite cells accompany neuronal cell bodies in ganglia, and Schwann cells ensheath axons and form their myelin sheaths. In the CNS oligodendrocytes form myelin, and astrocytes fill in all the spaces between neurons and their processes. Microglia are small cells throughout the nervous system that have functions similar to those of white blood cells of the monocyte/macrophage series.

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Development of the nervous system and common developmental abnormalities.


The nervous system develops from the embryonic ectoderm. The neural tube, formed by invagination of the neural plate and fusion of the neural folds, forms the whole CNS (except for the sacral and lower lumbar segments of the spinal cord).

The neural crest, derived from cells of the neural folds, develops into most of the PNS (neurons and glial cells). In addition, many neural crest cells give rise to non-neural tissues throughout the body. Some of the neurons in some cranial nerve ganglia are not of neural crest origin but derive from placodes, which are localized thickenings of the ectoderm of the embryonic head. The olfactory epithelium and the sensory receptors of the inner ear also arise from placodes.
Diagram of the events of neurulation
Neural tube

Length of the spinal cord.

The vertebral column elongates more than the spinal cord. Consequently the adult cord ends at the level of vertebra L2. Below that level the vertebral canal contains the cauda equina, which consists of the roots of the lower spinal nerves and the filum terminale. The filum terminale is the stretched-out remnant of the embryonic tail.   Growth of the spinal cord
Growth of spinal cord

Basal and alar laminae.

There are two populations of young neurons in the neural tube, these forming the basal lamina ventrally and the alar lamina dorsally. At the level of the spinal cord, these laminae become, respectively, the ventral and dorsal horns of the spinal grey matter. The ventral horn contains motor neurons whereas the dorsal horn receives the incoming axons of primary sensory neurons.

At the level of the medulla and pons, the roof plate expands to form the wide, thin roof of the fourth ventricle. Consequently neurons derived from the alar lamina come to occupy the lateral part of the floor of the 4th ventricle, and those derived from the basal lamina are medially situated.  (Alar and basal laminae) 
Alar & basal laminae
In the medulla and pons, motor nuclei of cranial nerves are therefore located medially whereas sensory nuclei are located laterally. (A nucleus is a cluster of similar neuronal cell bodies in the CNS.)

Development of the cerebrum.

Even before the neural folds begin to fuse (Day 18 after fertilization) the future cerebral hemispheres, brain stem and spinal cord are evident. The rostral and caudal neuropores close on Days 23 and 27 respectively, and by Day 28 all the major parts of the brain are in place. (From 8 weeks onward the embryo is called a fetus. The fetal period is characterized mainly by growth rather than the formation of organs.)
Longitudinal section of 22-day embryo showing the neuropores

The enlargements of the rostral end (initially the rostral half) of the neural tube are the hindbrain, midbrain and forebrain. Flexures in the developing brain serve to (a) accommodate the tubular brain in a round cranial cavity, and (b) allow for the optical axes of the eyes to be at right-angles to the long axis of the body.
Development of the cerebral hemisphere
Devel. of hemispheres
At 11 weeks the main lobes of the cerebral hemisphere are present, but most of the sulci and gyri have yet to form. Enlargement of the cerebral and cerebral cortex proceeds during the remainder of the fetal period. Growth of the brain continues into childhood, with most of the increase in volume being due to myelination of axons and proliferation of dendrites (associated with increasing numbers of synapses).

Progeny of neural crest cells.

Neural crest cells that remain alongside the vertebral column become the neurons and glial cells of sensory and autonomic ganglia. Those that migrate along the courses of growing axons become the Schwann cells of nerve roots and nerves and the cells associated with specialized peripheral nerve-endings.

Other neural crest cells migrate more extensively. Some become the endocrine cells of the adrenal medulla; others form the melanocytes in the skin. Many cranial neural crest cells differentiate into bones and muscles of the head.

Common abnormalities of development of the CNS.

Failure of neuropore closure: Anencephaly if it's the anterior neuropore; myeloschisis if it's the posterior neuropore that fails to close. Most types of spina bifida are due to failure of development of vertebral laminae in the lumbar region. The overlying skin and muscles may be present (spina bifida occulta) or they may be missing (meningocoele or meningomyelocoele). Some drawings of developmental abnormalities follow.

Spina bifida 2 types of cystic S.B. Myeloschisis Cranial defects Anencephaly Chiari malformation

Internal hydrocephalus: Cerebrospinal fluid (CSF) fails to escape from the ventricles, which expand. A common type is due to closure of the cerebral aqueduct. There are malformations that include both hydrocephalus and spina bifida. The Chiari malformations are the most common.


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Organization of the peripheral nervous system: roots, nerves and ganglia.

In man and in all other vertebrate animals, the nervous system has two divisions: the central nervous system (CNS) is contained in the axial skeleton, and the peripheral nervous system (PNS) is distributed through most of the other parts of the body (Plan of the whole human nervous system).

The central nervous system is connected to other parts of the body by nerves. Neuronal cell-bodies outside the central nervous system occur in ganglia (singular, ganglion). The spinal nerves are segmentally organized. Each has a dorsal and a ventral root, separately connected with the spinal cord. The dorsal root bears a ganglion (called either a spinal ganglion or a dorsal root ganglion); the ventral root does not. The dorsal roots are exclusively sensory in mammals, whereas the ventral roots contain the axons of motor neurons and the axons of neurons that control internal organs, blood vessels, and glands.

Paired cranial nerves connect the brain with other structures. The olfactory nerves, concerned with smell, enter the olfactory bulb, which is at the rostral end of the telencephalon. The optic nerves, like the retinas of the eyes, are made of central nervous tissue. They are therefore not real nerves but outgrowths of the brain. The remaining cranial nerves emerge from the brain stem, which consists of the midbrain pons and medulla.

Segmental organization

The nervous system develops from embryonic segments, but in the adult state this is obvious only in the connections of nerve roots with the spinal cord.

The formation of a spinal nerve is illustrated in Spinal nerve. This diagram also shows structural elements that will be referred to later in this Section.
A segment
Spinal nerves have numbers derived from the vertebrae. The highest spinal nerve penetrates the atlanto-occipital membrane, above the arch of the atlas, which is the first cervical vertebra or C1. The second cervical nerve passes between the atlas (vertebra C1) and the axis (C2). There are 7 cervical vertebrae. The lowest cervical nerve is therefore C8. Cervical nerves 1 to 7 go through foramina above the numbered vertebrae. The roots of nerve C8 pass below the arch of vertebra C7 and above that of T1. All the thoracic (T1 - T12), lumbar (L1 - L5) and sacral (S1 - S5) nerves go through foramina below the equivalently numbered vertebrae. To complete the story, a single coccygeal nerve overlaps with S5 in supplying the perianal skin.

The most obvious consequence of the segmental organization of the spinal nerves is seen in the Dermatomes, which are bands of skin that run horizontally on the trunk and lengthwise on the limbs (Dermatomes).
Each dermatome is centered on the distribution of axons from a single dorsal root ganglion, but each ganglion also supplies skin in the dermatomes above and below its own level. Consequently, it is necessary to transect three adjacent dorsal roots or spinal nerves in order to completely denervate the skin of one dermatome. Transection of a single spinal nerve, or destruction of its ganglion, diminishes but does not abolish sensation in the affected segment of skin. The cutaneous lesions of herpes zoster, a common virus that infects certain pain-responsive neurons in individual sensory ganglia, often neatly map the distributions of dermatomes and also illustrate the extension of innervation into the adjacent segments of skin. The nerve supply to the skin of the limbs is delivered by cutaneous nerves that are formed in limb plexuses (brachial and lumbosacral) by complex interchanging and mixing of fibers from different spinal roots. The areas supplied by cutaneous nerves bear little resemblance to the dermatomes. They are sharply demarcated, with little or no territorial overlapping (Dermatomes). The widely overlapping dermatomes cut across adjacent areas of skin supplied by cutaneous nerves. A cutaneous nerve lesion, such as an injury or a mononeuropathy, results in a well defined area of defective sensation, and anatomical knowledge can be used to identify the affected nerve.

Most of the skin of the head is supplied by the three divisions of cranial nerve V. The areas are sharply demarcated, and therefore do not correspond to dermatomes. Cranial nerves VII, IX and X supply small, overlapping areas of skin of the external ear, and the dermatome of the second cervical nerve includes parts of the head, ear, face and neck. (The first cervical nerve lacks a dorsal root in most people.)

Muscles receive motor and sensory innervation. Most of the muscles of the limbs are supplied nerves formed in the limb plexuses from two or more roots. Table 6 (Segmental landmarks) shows the segmental innervation of a few clinically important muscles. A stretch reflex (tendon jerk) requires the integrity of both the motor and the proprioceptive sensory innervation of the muscle.

Table 6.    Useful landmarks of human skin and muscle innervation

Skin Muscles (and stretch reflexes)
C2 Occipital region of head    
C5 Tip of shoulder
(The top of the shoulder is in the C4 dermatome)
    C5-C6 Flexion of elbow (Biceps jerk)
C6 Thumb    
    C7-C8 Extension of elbow (Triceps jerk)
C8 Little finger C8-T1 Small muscles of hand
Oppose thumb to fingers; hold piece of paper between adjacent fingers
T4-T5 Nipple    
T10 Umbilicus    
L3 Front of knee L2-L3 Quadriceps (Knee jerk)
L5 Big toe    
S1 Little toe, heel S1-S2 Calf muscles (Ankle jerk)
S3 and below Genitalia and anal area    

Relation of spinal cord and nerve roots to the vertebral column

The vertebral column is longer than the spinal cord, which ends at the level of the upper border of vertebra L3 in the newborn and at the upper border of vertebra L2 in the adult. The lower spinal nerves must therefore course caudally before passing through their corresponding intervertebral foramina.  Immediately below the caudal end of the spinal cord, the neural canal contains the roots of nerves L2-L5, S1-S5 and the coccygeal nerve. Intervertebral foramina

A lesion arising from the axial skeleton, such as a herniated intervertebral disk or tumor tissue from a vertebral body or pedicle, can press on the spinal cord or spinal nerves. The consequences depend on the level of the involved disk or vertebra. In the cervical and upper thoracic spine there is little discrepancy between the spinal segments and the vertebrae. There is little free space in this part of the neural canal, so a lesion is likely to impinge on the cord as well as on a spinal nerve. The body of vertebra T10 is level with spinal cord segment T11. Below this level, the discrepancy between vertebral and spinal levels increases rapidly, because the lower lumbar and the sacral segments of the spinal cord are much shorter than the cervical and thoracic segments. All the spinal cord segments below T11 are in the range of just three vertebrae, T12, L1 and L2.

The foramina are above the levels of the intervertebral disks. Consequently, a herniated disk below C7 cannot compress its own segmental nerve; it presses on the nerve one or two segments lower. For example, an L4-5 disk herniation commonly compresses spinal nerve L5 or S1, causing pain and other sensory abnormalities in the appropriate dermatomes (see Dermatomes figure).

Cranial nerves

Although the brain stem develops from segments (known as neuromeres), their peripheral distributions and central connections are most easily understood in terms of the functions of each nerve. These are set out in Table 7. Note that the second cranial "nerve," despite its traditional name, is not a nerve but an outgrowth of the brain, as is the retina.

Table 7.     Functions of the cranial nerves.

This table includes functional components that can be tested by clinical examination or that cause symptoms if affected by disease. Physiological afferents from internal organs¹ are omitted from the table.

  Functional components
Cranial nerve Motor (= supplying skeletal muscle) Preganglionic parasympathetic² General sensory (skin, mucous membranes) Special senses
I     Olfactory       Smell
II    Optic       Vision
III   Oculomotor Eye movements other than those mediated by IV & VI. Elevation of upper eyelid Constriction of pupil (ciliary ganglion)    
IV    Trochlear Certain downward eye movements      
V     Trigeminal Muscles that open and close the mouth; tensor tympani muscle of middle ear Skin of face; mouth, teeth, nose, sinuses, dura mater of anterior and middle fossa    
VI    Abducens Abduction of eye      
VII   Facial Muscles of face; stapedius muscle of middle ear Lacrimal and nasal glands (pterygopalatine ganglion); sublingual & submandibular salivary glands (submandibular ganglion) Part of external ear and tympanic membrane Taste: palate & anterior two thirds of tongue
VIII  Vestibulocochlear:
IX    Glossopharyngeal Stylopharyngeus muscle Parotid gland (otic ganglion) Pharynx, middle ear, posterior third of tongue Taste: posterior third of tongue
X     Vagus Muscles of larynx & pharynx Slows heart (cardiac ganglia); increases gastric acid secretion and empties stomach (enteric nervous system) Larynx, trachea, oesophagus, dura of posterior fossa; part of external ear and tympanic membrane Taste: epiglottis
XI    Accessory³ (Spinal component) Trapezius and sternocleidomastoid muscles      
XII   Hypoglossal Muscles that move the tongue      

Footnotes to Table 7

¹ Afferent fibers in IX and X are of great importance for regulation of cardiovascular and respiratory function, but they do not give rise to conscious sensations, and the physiological functions are not usually disturbed by unilateral lesions that affect the nerves or their central connections.

² The names of the parasympathetic ganglia are indicated in parentheses after the functions.

³ The small cranial root of XI carries motor axons destined mostly for the larynx. These cross over into X by way of a communicating branch, as the two nerves pass through the jugular foramen in the base of the skull. The fibers of the spinal root have their cell bodies in segments C1-C5 of the spinal cord.

Autonomic nervous system

Skeletal muscles are supplied by motor neurons whose cell bodies are in the spinal cord (anterior horn) or brain stem (motor nuclei of cranial nerves). In contrast, glands, cardiac muscle, and the smooth muscle of blood vessels and internal organs are supplied by neurons in ganglia of the autonomic system. These ganglia receive afferent preganglionic fibers, which are the thinly myelinated axons of neurons in the spinal cord or brain stem. The neurons in the ganglia have unmyelinated axons, the postganglionic fibers that innervate smooth and cardiac muscle and secretory cells. There are three divisions of the autonomic system: sympathetic, parasympathetic and enteric.

The ganglia of the sympathetic system are the chains of paravertebral ganglia that lie on the lateral aspects of the bodies of the vertebrae, and also the preaortic or collateral gangliaassociated with the branches of the aorta that supply abdominal organs. There is a sympathetic chain ganglion for every spinal nerve. Postganglionic fibers enter the nerve by way of a gray ramus communicans (Formation of spinal nerve) and are distributed to blood vessels, sweat glands and the little muscles that move hairs. Blood vessels of the skin constrict in response to their sympathetic supply, whereas those in muscles dilate. Some of the ganglia for the nerves C1 to T1 are fused; consequently there are only three cervical sympathetic ganglia. In most people there is a stellate ganglion, formed from inferior cervical (C7-C8) and first thoracic ganglia. The middle cervical ganglion is connected with nerves C5 and C6. Postganglionic fibers from the large superior cervical ganglion (C1-C4) accompany the carotid artery and its branches. Some enter the eye, where they supply the dilator pupillae muscle of the iris. Others supply smooth muscle within the upper eyelid1. All three cervical ganglia send postganglionic fibers into cardiac nerves, which run alongside the common carotid artery and aorta and supply the muscle of the heart. Increased activity of the sympathetic system increases the rate and force of contraction of the heart.
In the absence of active sympathetic innervation of the eye, orbit and face, the pupil constricts (unopposed parasympathetic action), the upper eyelid droops partly, but can be raised voluntarily (intact oculomotor nerve innervation) and sweating does not occur on the affected side of the face. These changes (Horner's syndrome) can result from damage to the superior cervical ganglion, its pre- or postganglionic fibers, (which pass through the stellate ganglion), or to transection of descending axons in the lower brain stem or spinal cord that control the preganglionic neurons.
Preganglionic sympathetic neurons are present only in spinal cord segments T1 to L2, where they occupy the lateral horn of the gray matter. Their myelinated axons constitute the white rami communicantes (see figure), which are associated only with nerves and ganglia T1-L2. Preganglionic fibers destined for sympathetic ganglia above and below these levels pass rostrally and caudally in the sympathetic trunk, which interconnects all the ganglia of the sympathetic chain. Some preganglionic fibers pass through thoracic sympathetic ganglia and emerge as the roots of the greater (T5-T9), lesser (T10-T11) and lowest (T12) splanchnic nerves. These nerves pass behind the diaphragm and end in the preaortic ganglia. Some go to the adrenal medulla (which is a sympathetic ganglion modified to secrete its transmitter into the blood). The efferent axons from the preaortic ganglia accompany blood vessels to abdominal organs, where most end by synapsing with neurons of the enteric nervous system (see below).

Parasympathetic ganglia are found in the head, connected with certain cranial nerves, and associated with the walls of thoracic and pelvic viscera. Preganglionic fibers leave the brain stem in cranial nerves III, VII, IX and XI and terminate in cranial parasympathetic ganglia. The neurons in these ganglia supply the structures whose functions are stated in Table 7.The cardiac ganglia receive their preganglionic afferents from the vagus nerve; their neurons supply cardiac muscle cells, principally in the atria. The pelvic splanchnic nerves, branches of S2, S3 and S4, carry preganglionic fibers to the parasympathetic ganglia that supply the detrusor muscle of the urinary bladder and the blood vessels of erectile tissue in the genitalia.

The enteric nervous system consists of thousands of tiny, interconnected ganglia in the walls of the alimentary canal, from esophagus to anus, and of some of its associated structures such as the biliary system and pancreas. These ganglia, which supply the smooth muscle and secretory tissues of the gut, contain several types of neurons, with a wide variety of neurotransmitters. The enteric nervous system can do much of its work independently, but it is modulated by preganglionic fibers from the vagus nerve (to the stomach, small intestine and first half of the colon) and from the pelvic splanchnic nerves (distal colon and rectum). Parasympathetic activity stimulates propulsion of the contents of the gut. Of the vagal fibers that enter the abdomen, a majority end in enteric ganglia of the stomach, and the integrity of this preganglionic supply is essential for acid secretion and for opening of the pyloric sphincter.

Most of the postganglionic sympathetic fibers from the preaortic ganglia synapse with neurons in enteric ganglia, but some contact blood vessels and a few supply intestinal smooth muscle. Activity of the sympathetic system causes constriction of visceral blood vessels and retards propulsion of the contents of the alimentary canal.


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Anatomy of the spinal cord.

The spinal cord is shorter than the spinal canal in which it is suspended. Except in the neck, spinal cord segments are rostral to the corresponding vertebrae. The end of the adult spinal cord (the conus medullaris) is level with the 2nd lumbar vertebra.

Lumbar puncture: Cerebrospinal fluid can be sampled by a needle put into the subarachnoid space below the level of the conus medullaris.

The cross sectional area of the central gray matter indicates the number of neurons: largest for segments supplying limbs.
       (Different levels)
The cross sectional area of the white matter decreases caudally because there are fewer descending and ascending fibers.

Motor neurons are in the ventral horn; sensory axons enter the dorsal horn and the dorsal funiculi. Preganglionic autonomic neurons are laterally placed, in segments T1-L2 and S2-S4.

Section of a thoracic segment of the spinal cord showing major groups of neurons in the grey matter, and positions of tracts in white matter.
Spinal cord
Ascending tracts include the uncrossed gracile and cuneate fasciculi (from sensory ganglia) and the crossed spinothalamic tract (from the dorsal horn). These are concerned with different types of sensation.

Descending motor tracts include the uncrossed vestibulospinal and the crossed lateral corticospinal tract. Hypothalamospinal and some reticulospinal fibers influence autonomic functions.

Lesions in different parts of the spinal cord produce sensory and motor abnormalities appropriate to the functions of the tracts that have been transected. The segmental level of a lesion is indicated by the affected dermatomes and movements.
Lesion causing the Brown-Sequard syndrome  Can you determine what the motor and sensory deficits are, for parts of the body below the segmental level of the lesion?

Spinal reflexes.
A reflex has afferent and efferent limbs. The simplest one is the stretch reflex, see diagram. This includes only one synaptic interruption. Branches from the axon of the proprioceptive neuron directly contact motor neurons for the same muscle.
Stretch reflexDescending pathways generally suppress stretch reflexes. If descending motor pathways are severed, by disease or injury, the resulting spasticity of the paralyzed muscles is due to uninhibited stretch reflexes.


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The cerebral cortex: anatomical landmarks and location of primary sensory and motor areas.

It is easy to get bogged down in the names and positions of sulci and gyri. Start with those that are easily seen, and don't bother with ones that are not listed here.

Longitudinal (interhemispheric) fissure Between the cerebral hemispheres. Its floor is the corpus callosum.
Lateral sulcus (sylvian fissure) Separates temporal lobe from frontal and parietal lobes
Insula Landmark for underlying lentiform nucleus
Central sulcus Landmark for primary motor and somatic sensory areas
Frontal lobe  
    Precentral gyrus Primary motor area
    Inferior frontal gyrus Includes Broca's expressive speech area
    Prefrontal cortex Complex functions involving foresight
    Anterior cingulate cortex Memory; movement
    Premotor area Control of movement
    Supplementary motor area Initiation of movements
    Frontal eye field Saccadic eye movements (not pursuit or vergence)
Parietal lobe  
    Postcentral gyrus Primary somatosensory area
    Superior parietal cortex Somatosensory association area; lesions cause apraxia, neglect
    Inferior parietal cortex Higher order association areas for language, calculation; lesions cause receptive aphasia
    Posterior parietal cortex Higher order association area for vision; eye-field for pursuit movements
Occipital lobe  
    Calcarine sulcus
    (and the adjacent gyri)
Primary visual area
    Remainder of the occipital lobe Visual association cortex
Temporal lobe  
    Inferior and inferolateral
Highest order visual association area, including memories of complex scenes
    Superior temporal gyrus:  
        Anterior & middle part
        of superior surface
Primary auditory area
        Middle and posterior parts Auditory association area; also called Wernicke's area; part of the association area for language
    Parahippocampal gyrus:  
        Uncus Primary olfactory cortex
        Entorhinal area Includes primary and association cortex for olfaction. Afferents from all sensory association areas. Efferents to the hippocampus.
    Fusiform gyrus (lateral
    to collateral sulcus)
Includes visual association cortex for remembering people's faces
    Hippocampal formation
    (subiculum, hippocampus,
    dentate gyrus etc)
Integration of sensory experiences and formation of memories
Medial surface of hemisphere  
    The cingulate gyrus,
    cingulate sulcus and
    parieto-occipital sulcus
    are conspicuous landmarks.
The corpus callosum interconnects symmetrical areas of cerebral cortex of the two cerebral hemispheres

Functional areas of the cerebral cortex

Here is the Map

Cortical areas













This drawing shows the Somatosensory and motor homunculi


This classical picture of the homunculi, based on the work of Wilder Penfield in the 1930s and 1940s has recently been found to contain an error. The face should be upside down, but it is shown the right way up!
[See Servos P, Engel SA, Gati J & Menon R (1999). fMRI evidence for an inverted face representation in human somatosensory cortex. NeuroReport 10(7):1393-1395.]





BRAIN STEM ANATOMY    (Click here)


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This subject is covered in the practical classes. Students need to know the anatomy as shown by dissection and should also be able to identify the structures seen in:
(a) A horizontal slice at the level of the insula and internal capsule. (b) A coronal slice at the level of the insula and internal capsule.


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Arteries of the central nervous system and the regions they supply.

The vasculature of the CNS is adequately described in the "Manter & Gatz" textbook, with rather more details than are needed for Anatomy 530a.

The arteries at the base of the brain anastomose in the circle of Willis (circulus arteriosus, arterial circle).
The arteries forming the circle, and the branches that supply the brain, can be summarized in a simple thumbnail diagram, which is easily learned. Brain arteries - thumbnail diagram  Click here for a labelled version of this simple diagram.
Circle of Willis
 Click here for an unlabelled colour photo that shows most of the arteries at the base of the brain.

The brain is supplied by 4 arteries. On each side:
    The internal carotid artery enters the skull through the carotid canal and then traverses the cavernous sinus (= lateral parasellar compartment).
    The vertebral artery (a branch of the thyrocervical trunk of the subclavian artery) passes through foramina in the transverse processes of cervical vertebrae, pierces the atlanto-occipital membrane, and enters the cranial cavity by way of the foramen magnum.
Picture of the inferior surface of the brain with arteries labelled.
In this illustration the groups of central arteries that supply the internal parts of the cerebral hemispheres are clearly shown but are not labelled.
The central arteries are proximal branches of the three cerebral arteries and branches of the posterior communicating arteries.  The lenticulostriate arteries (from the middle cerebral) supply the internal capsule.
The three cerebral arteries supply the cortex: Anterior cerebral: Medial surface and top of hemisphere, excluding occipital lobe.
Posterior cerebral: Occipital lobe, inferior surface of temporal lobe; also amygdala, hippocampal formation.
Middle cerebral: Most of the lateral aspect of the hemisphere - frontal, parietal and temporal lobes.  Also, in the subcortical white matter, association fibres (notably the arcuate fasciculus) and projection fibres (notably the geniculocalcarine tract).
The vertebral and basilar arteries send branches to the brain stem and cerebellum. The posterior inferior cerebellar artery supplies the lateral part of the mid- and upper medulla in addition to the cerebellum.
The caudal medulla and spinal cord are supplied by branches from the vertebral arteries.
The labyrinthine artery, usually a branch of the anterior inferior cerebellar, supplies the inner ear.

Note the position of the oculomotor nerve, medial to the uncus and also in the angle between the posterior cerebral artery (which supplies structures above the tentorium cerebelli) and the superior cerebellar artery (which supplies structures below the tentorium).
If the cerebrum is pushed downward (by an expanding intracranial haemorrhage or tumour, for example), there is pressure on the nerve (What happens?), and the posterior cerebral arteries can be stretched over the free edge of the tentorium and occluded. What are the expected effects of bilateral PCA occlusion?

Venous drainage and the absorption of CSF.
Superficial cerebral veins traverse the subarachnoid space and then pierce the dura as they enter intracranial (dural) venous sinuses. The diagram shows 2 veins entering the superior sagittal sinus.
   Head injury (rapid rotation of brain within cranium) can tear veins as the traverse the dura, causing subdural haemorrhage.
   The arachnoid granulations allow cerebrospinal fluid to flow into the venous blood of the sinus but prevent back-flow of blood into the subarachnoid space (a valve mechanism).

Click here for a full sized image

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Somatic sensory pathways.

Neuronal signals from skin and deeper structures are segregated in the spinal cord. Transmission to the thalamus and cerebral cortex may occur through the spinothalamic tract or through the dorsal funiculi and medial lemniscus.

For pain, temperature and the less discriminative aspects of touch, neurons in the dorsal horn have axons that cross in the spinal cord and ascend as the spinothalamic tract, which is laterally situated in the spinal cord and brain stem.

For discriminative touch and for conscious proprioception, the axons of primary sensory neurons ascend ipsilaterally in the dorsal funiculus (either gracile or cuneate fasciculus) and end in the gracile or cuneate nucleus. Fibers arising in these nuclei cross in the medulla and ascend in the medial lemniscus, which is near the midline in the medulla and shifts to a lateral location in the midbrain.
      For conscious proprioception from the lower limb there is an additional pathway, involving the dorsal spinocerebellar tract and nucleus Z in the medulla.

Spinal cord

Reminder - Positions of tracts in spinal cord

Click here to download sompaths.exe (311073 bytes).  This is a free-standing executable slide-show - the one used for the lecture. (This needs MS Windows 95 or later. Sorry about that. If you use an older computer, I can provide plenty of DOS-based software that's much better than this Windows stuff, but some of it won't run on computers made since 1998-99. Ask me if you're interested. None of my downloadable programs are for Mac computers.)

The differences between the two main ascending somatosensory pathways are important functionally and clinically.

The medial lemniscus system (= dorsal column system = dorsomedial system) is for discriminative touch and conscious proprioception.
   The pathway ascends ipsilaterally in the dorsal white matter of the cord, and crosses in the caudal (closed) medulla.
   In the medulla the medial lemniscus is close to the midline; the tract moves laterally as it ascends through the pons and midbrain.
The spinothalamic system (= anterolateral system) is for simple touch, warmth, cold and pain.
   The pathway crosses the midline immediately and ascends in the lateral and ventral white matter of the spinal cord.
   The spinothalamic tract maintains a lateral position as it traverses the medulla, pontine tegmentum and midbrain.

Both the spinothalamic tract and the medial lemniscus terminate in the ventral posterior nucleus of the thalamus. This thalamic nucleus projects to the primary somesthetic cortex of the postcentral gyrus, where the contralateral half of the body is represented as an upside-down homunculus. Homunculi
Somatosensory pathways Diagram summarizing the somatic sensory pathways

The somatic sensory pathways for the head involve the trigeminal sensory nuclei and their projections to the contralateral VPM thalamic nucleus.
      Primary afferent fibers for touch end in the pontine trigeminal nucleus. Pain and temperature fibers descend in the spinal trigeminal tract before ending in the caudal part of its nucleus. This pathway will be discussed later, in connection with the central connections of cranial nerve V.

Lesions in the spinal cord and brain stem can affect the somesthetic pathways separately, causing dissociated sensory loss.
What sensory loss results from a destructive in the lateral part of the medulla, involving the left spinothalamic tract and sensory nuclei of the left trigeminal nerve (but sparing other somatic sensory pathways)?    Click here for the answer (but think first!)

Wallenberg's syndrome lesion

The main pathways are supplemented by others, especially for pain, which involve the reticular formation and thalamic nuclei other than the VPL or VPM .

The cerebral cortex is necessary for localizing the source of a painful stimulus and for the recognition of objects by touch.

A note about nuclei in sensory pathways.

The synapses between the main neurons in a pathway are not simply "relays," which would serve no useful purpose. Through connections from other parts of the CNS, and with the involvement of local interneurons, the incoming signals are modified for onward transmission.
For example:
In the gracile and cuneate nuclei, lateral inhibition (feed-forward and feedback types) sharpens the perception of the most strongly stimulated part of a receptive field. There is also remote inhibition by corticobulbar fibres in these nuclei. In the dorsal horn of the spinal cord, large and small diameter axons contact inhibitory interneurons and tract cells that send pain signals to the thalamus. Balance between the two types of input constitutes the gate control mechanism for pain.

Descending pathways that influence sensation

The proper interpretation of the outside world and the state of the body itself would be impossible if every impulse in every sensory axon were to be brought eventually to the cerebral cortex. An editing system is necessary, so that the cortex can select the sensory information worthy of conscious attention while leaving more humble duties to the spinal cord, brain stem, and cerebellum. The editing function is carried out by descending fibres that terminate in the sites of origin of the ascending tracts. Some of these descending pathways are shown in a diagram (Click here).

Descending tracts modify activity in the ascending systems at three levels:
    1.  In the dorsal horn of the spinal gray matter. This is the site of termination of large numbers of corticospinal fibers, mostly from the postcentral gyrus. Other axons ending in the dorsal horn come from the reticular formation and from the gracile and cuneate nuclei. One of the reticulospinal projections, the raphespinal tract, is notable for inhibiting the upward transmission of signals concerned with pain. It originates in the raphe nuclei, in the midline of the medulla, and the unmyelinated serotonergic axons of the tract are lateral to the tip of the dorsal horn. The raphe nuclei are themselves stimulated by neurons in the periaqueductal gray matter of the midbrain. Electrical stimulation of the periaqueductal gray causes prompt relief of pain and has occasionally been done clinically for this purpose. A curious observation is that stimulation for a few minutes can produce analgesia lasting several hours.
    2.  In the brain stem. Large numbers of fibers descend from the somatosensory area of the cerebral cortex to the gracile and cuneate nuclei. They are presumed to influence the medial lemniscus system. Corticobulbar fibers also end in the trigeminal sensory nuclei.
The suffix "-bulbar" refers to the termination of axons in the brain stem. The term "corticonuclear" is sometimes used for axons of cortical neurons that end in nuclei of cranial nerves. However, many descending fibers that influence cranial nerves end near, but not within, the nuclei. The less precise term "corticobulbar" is therefore preferred.
    3.  In the thalamus. The VPL and VPM nuclei project to the first somatosensory area of the cerebral cortex. These thalamic nuclei also receive input from the same cortical areas.
(This isn't the only thalamocortical projection that is reciprocated; they all are.)


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DESCENDING MOTOR PATHWAYS   (Click here)  for some notes.


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THE CEREBELLUM   (Click here)  for some notes.

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THE BASAL GANGLIA   (Click here)  for some notes.

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Some cranial nerves concerned with special senses, and their central connections:

   I        Olfactory system.

The olfactory system is presented as a 15-minute videotape entitled "The Rhinencephalon" by D. G. Montemurro. This tape, shown in the lecture, is also available in the Taylor (Sciences) Library.
The following three images summarize the system. For Anatomy 530a you do not need to know about cells in the olfactory epithelium other than the receptor neurons.
Location of olfactory epithelium, nerves and bulb
Nose and olfactory structures
Structure of the olfactory epithelium (annotated diagram) Destinations of fibres of the olfactory tract
Olfactory pathway

   II      Visual system.

Damage to the visual pathways can result in visual field defects, with the site of a lesion determining which part of the visual fields is blind. To understand the visual pathways it is first necessary to be familiar with the geometrical optics of the eye, and to appreciate that (a) images projected onto the retina are inverted, both left-right and top-bottom, and (b) in man, both eyes are directed forwards, so that almost all the visual field is projected onto both retinas. It is also necessary to know that there is retinotopic organization throughout the pathways.
The notes below relate to images. Click the links on the right side of the table to look at the images (which are the ones shown in the lecture).
Anatomy and optics of the eye.
A horizontal section through the left eye, viewed from above, showing the focusing of a real, inverted image on the retina.
Behind the lens, the eyeball is filled by the vitreous body, which is transparent and gelatinous. The space between the lens and the cornea is occupied by aqueous humour, a liquid secreted by the ciliary processes (anterior to ciliary muscle) and absorbed into veins at the angle between the iris and the cornea. The posterior chamber of the eye is between the lens and the iris; the anterior chamber is between the iris and the cornea.
The cells of the choroid contain a pigment, melanin, which prevents reflections of light within the eyeball. Melanin occurs also in the iris.
Anatomy and optical properties of the eye

Remember that the visual field is seen by both eyes (because they face forwards) and that an inverted image of the visual field is projected onto both retinas. It is necessary to know this in order to understand the topographical representation of different parts of the visual fields in the brain.

The retina is part of the CNS (outgrowth of the diencephalon), as is the optic "nerve."  The cellular organization of the retina is complicated. Diagram of retinal structure
[This diagram shows more detail than is required for Anatomy 530a]
The ganglion cells of the retina have axons that pass through the optic nerve to the midbrain and thalamus.
The fibres from the medial (nasal) halves of the two retinas cross the midline in the optic chiasma and go into the contralateral optic tracts.
The fibres from the temporal halves of the retinas go into the ipsilateral optic tracts.
The visual pathway (for conscious visual sensation)
Visual pathway

In addition to the lateral geniculate body there are at least 4 other destinations of fibres of the optic tract. These include the pretectal area for the pupillary light reflex and the superior colliculus which is involved in the control of eye movements.

This thumbnail drawing is helpful for working out visual field defects.
It can be used to solve all the classical visual field problems other than a Meyer's loop* lesion.
Visual pathways, thumbnail diagram Thumbnail diagram showing what crosses and what doesn't in the optic chiasma

The lens of the eye is shown in the thumbnail sketch to remind you that images on the retinas are inverted.

* Meyer's loop contains geniculocalcarine fibres that are deflected into the temporal lobe by growth of the temporal horn of the lateral ventricle. These fibres carry signals from the inferior halves of the contralateral hemiretinas. What visual field defect results from a destructive lesion in the right temporal lobe?  Try to work this on out yourself, as did Adolph Meyer (1866-1950), the Austrian ophthalmologist who deduced the topography of the geniculocalcarine projection.


   VIII  (cochlear).    Auditory system.

Sounds are detected by a receptor of great structural complexity, the organ of Corti in the cochlea of the inner ear.
Drawing that shows some anatomical features of the ear
Inner ear

The neurons in the spiral ganglion are bipolar (perhaps best considered to have two axons). Their distal processes receive synaptic input from cells of the organ of Corti. Their proximal processes form the cochlear nerve (= cochlear division of the vestibulocochlear nerve).
Axons of the cochlear nerve branch as they enter the medulla, and the branches end in the ventral and dorsal cochlear nuclei.
These small images show the locations of the vestibular and cochlear nuclei, and a few other landmarks.
Vestibular & cochlear nuclei and 4th ventricle Vestibular & cochlear nuclei in transverse section of rostral medulla Click here for a diagram of the auditory pathways
Auditory pathway
Level of transverse section of medulla = rostral end of the olive

Points to note about the central auditory connections.

1. There is more than one ascending pathway, and the number of synaptic interruptions between the organ of Corti and the primary auditory cortex is variable. Not all the nuclei of the pathways are shown in the diagram.
2. The ascending pathway from each ear is bilateral. Lesions above the level of the cochlear nuclei do not cause unilateral deafness.
3. Throughout the system there is tonotopic representation: in each nucleus and tract, cells and fibres are arrayed according to the frequencies of sound. (This begins in the cochlea, where high frequencies are detected at the base and low frequencies at the apex.)
4. Each superior olivary nucleus receives input from the left and right ventral cochlear nuclei. The timing and intensity of signals from the two ears are compared, and the resulting output of the superior olivary nucleus conveys stereophonic information to the inferior colliculus and in turn to the thalamus and cerebral cortex. Unilateral damage to the primary auditory cortex is said to impair recognition of the sources of auditory stimuli.
5. The primary auditory cortex (Heschl's convolutions) projects to the cortex of the posterior part of the superior temporal gyrus. This is auditory association cortex, and it interprets the patterns of received signals. In the left hemisphere this is Wernicke's area for recognizing spoken communication. In the right hemisphere the corresponding area processes non-verbal sensory input, including music.  The nearby parts of the parietal lobe (angular and supramarginal gyri) are also involved in recognizing and responding to complex auditory and other sensory experiences.

   VIII  (vestibular).  Vestibular system.

The vestibular apparatus is concerned with detecting position and movement of the head. It consists of the saccule, the utricle, and three semicircular ducts.  (Click here for an anatomical picture.  These are parts of a system of tubes and cisterns, the membranous labyrinth, that is entombed in the petrous part of the temporal bone. The membranous walls are separated from the lining of the bony labyrinth by perilymph, a fluid similar to CSF. The fluid inside the membranous labyrinth is endolymph, a liquid similar to intracellular fluid, with a high concentration of K+ and a low concentration of Na+
The sensory hairs of the receptor cells of the vestibular system (and of the organ of Corti) require an extracellular fluid of this unusual composition in order to work. Endolymph is secreted by the stria vascularis of the cochlear duct, and it is absorbed into the blood from the endolymphatic sac.
Vestibular organ

There are vestibular receptors of two types:

Static labyrinth. Otolithic organs in the utricle and saccule respond to the earth's gravitational force. The otoliths, being denser than endolymph, bend the sensory hairs downward. The direction of bending signals the orientation of the head in space. These receptors also respond to inertial movement of the otoliths, when the body accelerates or decelerates. Kinetic labyrinth. Receptors in the ampullae of the three semicircular ducts do not have otoliths but the sensory hairs are moved when there is movement (flow) of endolymph relative to the wall of the duct. This occurs with rotational movement of the head *.
*  When the duct moves, the endolymph doesn't, so the sensory hairs trail behind, in the same way that a fishing line is pulled by a boat moving through still water. The semicircular ducts are in planes mutually at right-angles  (Click here for a diagram), so rotation of the head in any direction will always induce some relative flow in at least one duct. The sensory hairs in each ampulla are deflected only when endolymph moves along the length of the duct. Detailed microanatomy and physiology of the vestibular and acoustic receptors are outside the scope of Anatomy & Cell Biology 350a and 530a.  It is, however, necessary to know about the static and kinetic components of the vestibular apparatus.
Vestibular receptors Click here for 3 drawings that show the structure of the receptors.

Clinical testing.  Irrigation of the earhole with either warm or cool water changes the temperature of the endolymph, which is only 2 or 3 millimetres away from the eardrum. Even a small temperature change sets up a convection current: warm endolymph flows up, or cold endolymph flows down. The ampullary receptors move with the flow;  it is as if the head were rotating in the opposite direction. 
In a conscious patient this causes vertigo and nystagmus. In a comatose patient the vestibulo-ocular reflex drives both eyes to look in a direction opposite to the simulated rotation of the head.
This simple clinical examination is called caloric testing. In its simplest form, it can show that the vestibular system (medulla) is functionally connected with the ocular motor system (midbrain) in a comatose patient, providing evidence that the patient is not "brain dead."
The tract that connects the vestibular nuclei to the oculomotor nuclei is the medial longitudinal fasciculus (MLF).
The MLF also contains fibres that interconnect the ocular motor (III, IV & VI) nuclei for making conjugate eye movements, but that's another story.

Central vestibular connections  are with the same side of the body and with the same side of the cerebellum.
Vestibular pathways
Click here for a larger diagram of the projections.


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The other cranial nerves:  III, IV and VI.

The three nerves that supply extraocular muscles contain somatic motor fibres. The oculomotor nerve contains, in addition, preganglionic parasympathetic fibres.
Oculomotor nerve supplies superior, medial and inferior rectus muscles, and the inferior oblique. It also supplies the levator palpebrae superioris (which raises the upper eyelid).

Trochlear nerve supplies only the superior oblique muscle.

Abducens nerve supplies only the lateral rectus muscle.

Extraocular muscles

Central connections. ("Deep origins")
First, remind yourself of the sites of emergence ("superficial origins") of the cranial nerves from the brain stem:  Lateral aspect    Ventral aspect    The nuclei of III, IV and VI near the levels of the emerging nerves.   (Click on the Lateral and Ventral links for larger diagrams.)
Brain stem from side Brain stem, ventral view
The Oculomotor nucleus is a complex of subnuclei, one for each muscle, located ventral to the periaqueductal grey matter, next to the midline, at the level of the superior colliculus.  The parasympathetic Edinger-Westphal nucleus is nearby.  Axons course ventrally, passing through the red nucleus.

The most conspicuous feature of a palsy that affects the motor component of III is that the eye is closed, because of paralysis of the levator palpebrae superioris muscle.

The preganglionic axons from the Edinger-Westphal nucleus end in the ciliary ganglion, which is behind the eyeball. The short ciliary nerves carry unmyelinated postganglionic fibres (axons of the neurons in the ganglion) to innervate smooth muscle: the sphincter pupillae (circular muscle fibres of the iris) and the ciliary muscle, which focuses the lens for near vision.
The preganglionic parasympathetic fibres are superficially situated in the nerve and are therefore the first ones to be affected by external pressure. The result is dilation of the pupil, with a sluggish or absent pupillary light reflex. A common cause of third nerve compression is a subdural haematoma pushing downward onto the convexity of a cerebral hemisphere. The uncus is pushed medially and it presses upon and stretches the oculomotor nerve of the same side.

The trochlear nucleus is caudal to the oculomotor nucleus, at the level of the superior colliculus. The axons of the motor neurons course caudally, dorsally and medially. They then decussate in the superior medullary velum and leave the dorsal surface of the brain stem below the inferior colliculus.
Thus, each superior oblique muscle is supplied by the contralateral trochlear nucleus. The only other muscle that receives comparable crossed innervation is the superior rectus: axons from the superior rectus subnucleus of the oculomotor complex cross the midline and join the third nerve of the opposite side.

A trochlear nerve palsy (due, for example, to diabetic neuropathy, or following a head injury) causes double vision on looking downward. The affected eye is slightly higher than the other (skew deviation), and the patient tilts the head to compensate.

The abducens nucleus is next to the midline in the floor of the 4th ventricle, at the level of the ponto-medullary junction. The motor axons pass ventrally.  In addition to motor neurons, the abducens nucleus contains internuclear neurons. These cross the midline, ascend in the contralateral medial longitudinal fasciculus, and end in the oculomotor nucleus, where they drive the motor neurons that supply the medial rectus. This arrangement provides for coordinated horizontal eye movements.
   The fibres of the facial nerve loop over the dorsal aspect of the abducens nucleus. The resulting lump in the floor of the 4th ventricle is called the facial colliculus.  Lesions in this region cause ipsilateral paralysis of the lateral rectus and facial muscles, and also failure of the contralateral medial rectus to adduct the eye. A lesion affecting VI outside the brain stem affects only the lateral rectus.

Click here  for an enlargement of the schematic diagram of the functional components of cranial nerves  III, IV and VI. 


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The other cranial nerves:  V, VII, IX, X, XI and XII.

In any peripheral nerve there are populations of fibres serving different functions. Each such population is a nerve component. For example, the oculomotor nerve has 2 components: motor and preganglionic autonomic. A nerve in a limb typically contains motor, somatic sensory and postganglionic autonomic components. In some of the cranial nerves there are also components related to the special senses, visceral sensory innervation, and preganglionic parasympathetic fibres (which are also "visceral").

The cranial nerve nuclei in the brain stem deal with the nerve components rather than the nerves.

For example:

First, remind yourself of the sites of emergence ("superficial origins") of the cranial nerves from the brain stem:  Lateral aspect    Ventral aspect   

Trigeminal nerve.  This is named for its three large divisions: the ophthalmic, maxillary and mandibular nerves. It has two components:

The central branches enter the pons in the large sensory root of the trigeminal nerve and are then distributed according to their functions:

Fibres concerned with touch end in the pontine trigeminal nucleus and in the rostral part of the spinal trigeminal nucleus.

Click here for a diagram of the central connections of the trigeminal nerve. V nuclei

Fibres concerned with pain and temperature turn caudally in the spinal trigeminal tract and end in the caudal part of the spinal trigeminal nucleus. (This is in the caudal half of the medulla and first two cervical segments of the spinal cord, where it blends into the dorsal horn.) The neurons for proprioception are exceptional. Their unipolar cell bodies constitute the mesencephalic trigeminal nucleus, which is lateral to the periaqueductal grey and extends rostrally to the level of the superior colliculus. The axons of these neurons form the mesencephalic trigeminal tract and are then distributed with the maxillary and mandibular divisions of V.  They go to muscle spindles, receptors in the temporomandibular joint, and pressure receptors around the roots of the teeth. (This pressure sense is related to proprioception; reflex connections to the motor trigeminal nucleus regulate biting and chewing.)
The cells of the mesencephalic trigeminal nucleus are the only primary sensory neurons to have their cell bodies in the central nervous system.

What sensory defect is caused by a lesion in the medulla that transects the spinal trigeminal tract?
Two disorders that affect the trigeminal nerve and ganglion are herpes zoster (= shingles) and trigeminal neuralgia (= tic douloureux). Usually one of the three divisions is involved.

Facial nerve.  This supplies the facial muscles and also has sensory and preganglionic autonomic components. The primary sensory neurons have their cell bodies in the geniculate ganglion. The functional components of VII are distributed in different branches of the nerve.

Click here for an enlarged diagram of the components of the facial nerve. C.N. VII
Facial paralysis When a facial paralysis is due to a lesion of the facial motor nucleus or of the nerve (a lower motor neuron lesion) all the muscles of the same side of the face are affected. (There may also be inadequate lacrimal or salivary secretion, or a localized taste deficit, depending on the exact location of the lesion.)  An upper motor neuron lesion affects only the lower half of the contralateral side of the face, for the reason explained in this diagram.

Glossopharyngeal nerve.  This too has motor, sensory and preganglionic components. Nuclei are shared with other cranial nerves, notably X.

Click here for enlarged diagram showing the central connections of the glossopharyngeal and vagus nerves.

Vagus nerve.  This nerve, like IX, has five components and two sensory ganglia. Its branches extend beyond the head and neck into the thorax and abdomen, hence the name (Latin vagus = wandering).

Click here for a diagram showing the central connections of the glossopharyngeal and vagus nerves.

Accessory nerve.  This is formed intracranially by the union of two roots.  (Click here to see a drawing of all the cranial nerve roots.)
All the fibres in both roots are motor. The spinal root contains axons of motor neurons that form a cell column, the accessory nucleus in the first 5 cervical segments of the spinal cord. The spinal root ascends in the subarachnoid space, enters the cranial cavity by way of the foramen magnum, and fuses with the cranial root.
C.N. XI The cranial root consists of the axons of some of the cells in the nucleus ambiguus, notably neurons that supply laryngeal muscles.
After fusion of the roots, the accessory nerve leaves the cranial cavity by way of the jugular foramen, alongside cranial nerves IX and X. The axons from the nucleus ambiguus then leave XI in its small internal ramus, which anastomoses with the vagus nerve. The larger external ramus of XI continues into the posterior triangle of the neck and supplies motor fibres to the trapezius and sternocleidomastoid muscles. (Click here for enlarged diagram of the components and roots of IX and its association with X.)

Disorders affecting IX, X and XI.  Damage to the motor neurons in the nucleus ambiguus or to their axons in branches of the nerves causes hoarseness (larynx) and unsymmetrical elevation of the soft palate (uvula deviates to the normal side). If the accessory nerve is injured in the neck the shoulder on the same side is lower (trapezius) and the head is turned towards the same side by the action of the contralateral sternocleidomastoid muscle. Upper motor neuron lesions do not affect the larynx and pharynx because the nucleus ambiguus receives bilateral afferents from the cerebral hemispheres. A hemispheric lesion typically causes weakness of the contralateral trapezius and the ipsilateral sternocleidomastoid - muscles that both move the face in the same direction.
Although IX is the conduit for much pain and discomfort in diseases of the throat and middle ear, sensory deficits in the territory of IX, X and XI are seldom encountered.
Disorders of parasympathetic functions of IX and X are also unusual. Surgical transection of both vagus nerves at the level of the diaphragm (vagotomy) suppresses gastric acid secretion and inhibits opening of the pyloric sphincter.

Hypoglossal nerve.  This is another nerve with a single, somatic motor component.
The cell bodies are in the hypoglossal nucleus, which is next to the midline in the caudal half of the floor of the 4th ventricle and extending caudally into the rostral part of the closed medulla. The axons innervate the extrinsic and intrinsic muscles of the tongue. C.N. XII Click here for a larger diagram.
In a lower motor neuron hypoglossal palsy the affected side of the tongue shrinks (denervation atrophy) and deviates to the paralysed side when protruded. In an upper motor neuron lesion (such as a hemispheric stroke) the tongue deviates to the weakened (contralateral) side but does not atrophy. There is partial bilateral descending control of the hypoglossal nucleus, so the effects of a upper motor neuron weakness are not severe and there is recovery.

How much of all this cranial nerve stuff do I really need to know for 350a? The only way to come to grips with the cranial nerves is to know the components and the associated nuclei, ganglia and functions. For a neuroanatomy course you are not expected to know the names and topographical details of the branches in the head and neck (though in the case of the facial nerve this information facilitates learning the functional components). You should know the neuroanatomical reasons for clinical abnormalities.

A useful exercise to test your knowledge is the following:  Set up a table with the functional components as the columns and the numbered cranial nerves as the rows. In each cell of the table write the names of nuclei, ganglia and functions. For example:
Motor Somatic sensory Special sensory Preganglionic
      III   Oculomotor nucleus, eye muscles except lat. rect. & sup. obl.      Edinger Westphal nucleus, ciliary ganglion, focusing & pupil constriction
      V   Motor trig. nuc. Masticatory & related muscles Face etc; 3 divisions; trigeminal ganglion, pontine & spinal V nuclei. Pain & temp. to spinal nucleus    
      IX   Nucleus ambiguus, stylopharyngeus only IX ganglia, pharynx, back of tongue, middle ear Taste, back of tongue  
      X         Nucleus ambiguus: cardiac ganglia. Dorsal nucleus of X: intrinsic neurons of stomach etc.
(Only a few cells have been filled in above, as examples. A column could be added for general visceral sensation, and the table could have rows for cranial nerves I, II and VIII.)


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Hypothalamus and pituitary gland.
[ For comfortable viewing of this section, your web browser window should occupy most of the width of the screen ]

Click here to download a diagram of hypothalamic
connections and functions. It's quite complicated
but might be helpful for revision.

Anatomical landmarks of the hypothalamus.

(Hypothalamic nuclei are projected onto a mid-sagittal section.)

Some neural connections of the hypothalamus.

Some hypothalamic neurons project directly to preganglionic neurons of the autonomic nervous system.

Regulation of body temperature is an important activity controlled by the hypothalamus.
Heat is produced by contracting muscles. The pathway is probably from the posterior hypothalamus to parts of the pontine and medullary reticular formation that give rise to motor reticulospinal fibres. Shivering is one way of raising a low body temperature.

The other hormone of the posterior lobe is oxytocin, named for its action of causing the uterus to contract.

Oxytocin also causes milk ejection, through a reflex initiated by suckling. The myoepithelial cells of the mammary gland contract, pushing the milk from the secretory units into the duct system. The circulating oxytocin also makes the uterus contract - an important event of maternal recovery following birth.

The hypothalamus, as well as the reticular formation of the brain stem, is involved in the sleep/waking cycle.

The mamillary bodies are part of the circuitry of the hippocampal formation.

The hypophysial (= pituitary) portal veins deliver high concentrations of hypothalamic releasing hormones to the anterior lobe of the pituitary gland.
(There are also hypothalamic release inhibiting hormones.)

The hypothalamic releasing hormones have names that end in -RH. For example, CRH for corticotrophin releasing hormone, and LHRH for luteinizing hormone releasing hormone.

Secretion of prolactin is controlled mainly by an inhibiting hormone, which is dopamine. Growth hormone secretion is controlled by GHRH and also by a release inhibiting peptide called somatostatin.

Benign tumours of the anterior lobe are quite common. Most do not produce hormones. Rarely a tumour secretes excessive amounts of a hormone. For example, an adenoma that produces growth hormone will cause gigantism in a child or acromegaly in an adult. Pituitary tumours enlarge in a rostral direction and presss on the optic chiasma, causing bitemporal hemianopia.




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Functional neuroanatomy of the prefrontal cortex, amygdala, and hippocampal formation. Disorders of the frontal and temporal lobes.

The prefrontal cortex (= prefrontal lobe) is the frontal cortex anterior to the areas specifically involved in motor control (including eye movements and speech). It includes the frontal pole and the orbital surface of the frontal lobe.

Diagram of connections of prefrontal cortex
Lesions that damage the prefrontal cortex bilaterally (or sever its connections with subcortical structures) cause a syndrome in which there is a profound personality change, with loss of the ability to predict consequences of actions or to adapt behaviour based on experience. The syndrome is attributable especially to loss of function of the orbital cortex and the cortex of the frontal pole. Other anterior frontal lesions can cause difficulty placing objects or ideas in correct sequences.
  Causes of prefrontal lobe dysfunction include trauma, surgery (prefrontal leukotomy), ischaemia, syphilis and Pick's disease.

The amygdala (= amygdaloid body) is inside the temporal pole - internal to the uncus, on the end of the tail of the caudate nucleus, and bulging into the temporal horn of the lateral ventricle. In a coronal section, the amygdala is seen as a mass of grey matter continuous with the cortex in the region of the uncus. The name amygdala is Latin for almond.

Diagram of connections of amygdala
Electrical stimulation of the human amygdala causes feelings of fear and sometimes also of anger. Increased neuronal activity can be demonstrated (by fMRI) in subjects shown emotionally evokative pictures.
  Destructive lesions in the human amygdala are associated with damage to the nearby hippocampal formation and visual association cortex of the temporal lobe.

The hippocampal formation is (for Anatomy 350a purposes) the same thing as the hippocampus as seen in dissected specimens.
The name hippocampus is Latin for sea-horse, probably applied to the appearance seen in a coronal section of the temporal lobe.
The hippocampus and dentate gyrus constitute a body of cerebral cortex with only one layer of neuronal cell bodies. In the subiculum the hippocampus merges with the 3-layered cortex of the entorhinal area, which is the anterior end of the parahippocampal gyrus. The name "entorhinal" means it's medial to the rhinal sulcus, which, in the human brain, is the anterior end of the collateral sulcus.  In rodents, rabbits and lowly mammals that eat worms and insects, the rhinal sulcus is the only visible indentation on the surface of the cerebrum, and the entorhinal area can account for one third or more of the cerebral cortex. The human entorhinal area (2 or 3 square centimetres) is much bigger than the equivalent area in little furry animals. Nevertheless, the entorhinal area and hippocampus are used by squirrels to survive in winter, by finding seeds and nuts that they have hidden. 
The connections of the hippocampus and the evidence for its involvement in memory were briefly reviewed in the notes for the previous lecture.

The amygdala, prefrontal cortex and hippocampal formation receive input, direct or indirect, from:
   (a) The association areas of the cerebral cortex.
   (b) The ventral tegmental area, which is a population of dopaminergic neurons in the midbrain, medial to the substantia nigra. The VTA also projects to the nucleus accumbens.
   The Mesolimbic system comprises these dopamine-secreting neurons in the midbrain that use their transmitter to modulate the activities of neurons in the amygdala, hippocapmus and prefrontal cortex.
   Schizophrenia is a mental disease in which there may be excessive action of dopamine in the "mesolimbic" parts of the forebrain. The disorder, which has various forms, is characterized by withdrawal from society, strange behaviour and speech, flattened affect, and commonly also auditory hallucinations and paranoia. The drugs used to treat schizophrenia antagonize the actions of dopamine.


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Neuroanatomy of language and memory.

Click here for a diagram showing association and language areas

Sensory association areas.

The primary sensory areas are connected by subcortical association fibers with the appropriate sensory association areas.

A primary sensory area receives information about the events reported by an ascending pathway, but it cannot recognize or appreciate the importance of the sensation. The higher functions of recognition and use of sensory data reside in areas of association cortex. These large areas, not always clearly defined, are adjacent to the primary sensory areas.

Thus the association cortex for general somatic sensation is posterior to the postcentral gyrus.
The association area for vision occupies the occipital lobe, together with the adjacent posterior parietal cortex and the inferolateral cortex of the temporal lobe.
The auditory association cortex is posterior to the primary area on the superior and lateral surfaces of the superior temporal gyrus.
The olfactory association area is the entorhinal cortex and the more posterior parts of the parahippocampal gyrus, together with part of the orbital cortex of the frontal lobe.

In addition to association fibers from the primary sensory areas, the sensory association areas receive projection fibers from several thalamic nuclei.

A large lesion in an association area causes difficulty with recognition of things that are heard, seen or felt. Disorders of the sensory association areas cause various kinds of agnosia. [Recognition of significance is gnosis (Greek for "knowledge").]

An agnosia may be visual, auditory, or tactile. The most common form of tactile agnosia is astereognosis, the inability to identify objects felt with the hand. The word astereognosis is also commonly used for inability to discern differences in shape and texture with the fingers. This symptom is usually due to a lesion in the contralateral parietal lobe, posterior to the hand area of the primary somaesthetic cortex.

Click here for diagram of somatic sensory areas and lesions that cause agnosias.

Language areas.

Cortical areas concerned with verbal and written communication, are in the temporal, parietal, and frontal lobes. These areas are concerned with language in only one of the hemispheres, usually the left.

Click here for diagrams of  the cortical language areas  and of  their interconnections.

The temporoparietal area is the receptive language area, which includes parts of the superior temporal, angular, and supramarginal gyri. Its integrity is necessary for the recognition of spoken and written words. The anterior part of this cortical region, which is the auditory association cortex, is called Wernicke's area, after Carl Wernicke (1848-1905), a German clinical neurologist. The receptive language area receives afferent fibers from the auditory and visual association areas of both hemispheres. It is also connected with the expressive language area in the left frontal lobe.

The expressive language area is often called Broca's area. It is in the frontal lobe, anterior to the lower end of the precentral gyrus.
Paul Broca (1824-1880), a French physician, was one of the first people to detect functional differences between the left and right cerebral hemispheres.
The integrity of Broca's area is necessary for producing speech to communicate ideas formulated in the mind.  The supplementary motor area is also essential for speech.

Disordered speech due to loss of function of cortical language areas is called dysphasia, or aphasia if the condition is very severe. These works have Greek roots meaning difficulty with or loss of speech.

A patient with receptive aphasia is not aware of talking nonsense and does so fluently. A patient with expressive aphasia, on the other hand, can hear the nonsense and recognize it as such, and keeps quiet (non-fluent aphasia).


Apraxia is clumsiness of movement due to cerebral cortical dysfunction. A typical cause is an infarct in the somatosensory association cortex in the medial part of the superior surface of the parietal lobe. This normally feeds signals related to proprioception to the motor cortex. Without properly processed proprioceptive input. Inaccurate instructions to the pontine nuclei, motor neurons etc result in clumsy movements of the contralateral hand.  Which artery supplies the medial part of the superior surface of the parietal lobe?

Click here for diagrams of  the motor cortical areas  and of  locations of lesions that cause apraxia etc.


It has long been generally agreed that memory for perceived facts and events is a function of the forebrain, and especially of the cerebral cortex.
If the word "memory" is more liberally interpreted, then it is a property of all parts of the brain, because neuronal activity everywhere is modified by earlier neuronal activity. It is possible to observe conditioned responses even in certain types of invertebrate animal that do not have anything equivalent to a brain. Memory can be displayed by cells that are not neurons, too. For example, the immune system responds more rapidly and intensely to previously encountered antigens than to antigens presented for the first time - the basis of immunization against infectious diseases, and the value of booster shots.

Experiments by Lashley (American psychologist) in the 1920s provided evidence against the involvement of specific parts of the forebrain in memory. He removed numerous parts of dogs' cerebral hemispheres and measured the resulting impairment of learned behaviour. The severity of the impairment increased with the amount of removed cerebral cortex, but was not related to which areas of cortex were removed. Lashley's conclusion:  Learning, storage and recall occur diffusely throughout the cortex.

In 1937 Kluver & Bucy (American neuropathologist & neurosurgeon) published a classic paper describing the effects of bilateral removal of the the temporal lobes in monkeys. Among other abnormalities, the animals lost the ability to learn new tricks. (This is just part of the Kluver-Bucy syndrome.) Later work, including studies of human subjects with bilateral temporal lobe lesions (from surgery and disease) indicated that the hippocampal formation was the part of the temporal lobe involved in learning. Through association fibres, the hippocampus can receive input from all regions of the cerebral cortex. The commonest disease that impairs recent memory is Alzheimer's - in which the earliest degenerative changes are in the entorhinal area and hippocampus. Memory deficits result also from bilateral lesions that interrupt the connections of the hippocampal formation.

The evidence for the hippocampi as parts of the brain essential for acquisition of memories is currently widely accepted, but it is also challenged by some greatly respected investigators. The challengers point out that bilateral hippocampal lesions are large and are always accompanied by damage to other parts of the cerebral hemisphere. Lashley might be right.
The postulated role of the hippocampus is in acquisition and short-term storage of remembered experiences. Long-term storage is not affected by bilateral hippocampal lesions or in the early stages of Alzheimer's disease. Procedural memory (for learned motor skills) resembles long-term memory in this respect.

Click here for two diagrams of hippocampal circuitry

Against Lashley's notion of disseminated memory storage:


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Examples of clinical diagnosis by application of neuroanatomical knowledge:

The consequences of an arterial blockage illustrate both the distribution of the artery and the functions of the structures it supplies.  By the end of a course in functional human neuroanatomy students should be able predict the effects of localized lesions and should be able to interpret the clinical symptoms and signs to determine the location of a lesion and, in typical examples, the identity of the obstructed artery.

(a) Cerebral artery occlusions.   Click here for a map of the cortical areas supplied by the three cerebral arteries. Arterial territories

Internal carotid artery.

This vessel is frequently obstructed by atheroma, which commonly gives rise to transient symptoms of cerebral ischaemia known as transient ischaemic attacks (TIAs). Complete, sudden obstruction cuts off most of the blood flow in the anterior and middle cerebral arteries.
Contralateral hemiplegia with sensory deficits. If on the left side (in 90% of people), severe aphasia.
There may also be blindness in the ipsilateral eye (ophthalmic artery) with loss of the temporal visual field of the contralateral eye (anterior choroidal artery supplies optic tract).
If the internal carotid artery is occluded after a prolonged period of progressive narrowing by atheroma, the anastomotic vessels at the base of the brain enlarge, so that the cerebral hemisphere receives blood from the contralateral side and from the vertebro-basilar system. Ischaemia may then be restricted to regions supplied by certain branches that do not receive adequate collateral perfusion. For example, a gradual internal carotid occlusion might cause infarction in the territory of anterolateral central branches of the middle cerebral artery that supply the posterior limb of the internal capsule.

Middle cerebral artery.

Occlusion of the vessel at its origin causes contralateral upper-motor-neuron paralysis of the upper limb and face, with global aphasia if left-sided. Lower limb functions are spared. Infarction of the geniculocalcarine tract, deep to the parietal cortex, results in contralateral hemianopia.
Obstruction of branches of the MCA results in fragments of the complete syndrome, such as monoplegia, upper motor neuron facial paralysis, or receptive aphasia.

Anterior cerebral artery.

Paralysis and sensory deficits in the contralateral lower limb and perineum. Urinary incontinence.
A proximal lesion - obstructing the origin of the anterior cerebral artery - causes hemiplegia affecting the limbs and lower face, because an early branch, the recurrent artery of Heubner, supplies the internal capsule. Proximal lesions may also cause ipsilateral anosmia from infarction of the olfactory bulb and tract.

Posterior cerebral artery.

Infarction of the occipital lobe causes contralateral hemianopia. Damage to the hippocampal formation results in a memory deficit, but this soon recovers. Bilateral posterior cerebral artery occlusions can result in a permanent inability to form new memories, in addition to blindness in both eyes.


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Examples of clinical diagnosis by application of neuroanatomical knowledge:
    (b) Brain stem strokes.

The vertebral and basilar arteries and their branches may be obstructed by atheroma or embolism. Often blockage of a larger vessel causes ischaemia only in the territory of a smaller branch. For example, the syndrome of occlusion of the posterior inferior cerebellar artery is often due to an obstructed vertebral artery.

Basilar artery thrombosis. Coma and decerebrate rigidity, soon followed by death from respiratory failure.
   (A large pontine haemorrhage results in sudden death.)

Basilar artery embolism. The embolus typically lodges at the terminal bifurcation of the basilar artery and obstructs the posterior cerebral and superior cerebellar arteries, including the central branches from the proximal part of the posterior cerebrals. Coma (from infarction of reticular formation of midbrain and rostral pons); diverging eyes with fixed, dilated pupils (bilateral infarction of fibres of III). In less severe cases there is recovery of consciousness, and the residual top of the basilar syndrome includes the oculomotor paralysis, together blindness or lesser visual field defects (occipital lobes) and disturbances of memory or behaviour (temporal lobes).

Wallenberg Posterior inferior cerebellar artery (PICA). (Wallenberg's syndrome) This is the commonest brain stem stroke. There is loss of pain and temperature sensation from the same side of the face (spinal trigeminal tract and nucleus) and from the contralateral limbs (spinothalamic tract); ipsilateral paralysis of vocal cord and palatal muscles (nucleus ambiguus); ipsilateral ataxia (inferior cerebellar peduncle), vertigo (vestibular nuclei), and an ipsilateral Horner's syndrome (due to interruption of hypothalamospinal or reticulospinal fibres destined for the preganglionic sympathetic neurons in the upper thoracic segments of the spinal cord).        [ This is a reproduction of Wallenberg's original (1908) drawing. ]
Click here for a photo of a Weigert-stained section of the medulla with annotations explaining the clinical features of a lateral medullary lesion.

Horner's syndrome, due to loss of sympathetic action on the eye, comprises miosis (small pupil), ptosis (drooping eyelid, but not closed as in a IIIrd nerve palsy) and apparent enophthalmos. (The eyeball appears further back in the orbit than the normal eye; this appearance is caused by the ptosis.)  Johann Friedrich Horner (1831-1886) was a Swiss ophthalmologist. His syndrome can have several different causes.

Anterior inferior cerebellar artery (AICA). Ipsilateral ataxia (cerebellum, middle cerebellar peduncle); vertigo and ipsilateral deafness (from inner ear infarction, the labyrinthine artery being in most people a branch of AICA).

Other brain stem syndromes.
Do not attempt to memorize the six examples that follow. Except in the case of Parinaud's syndrome, you should be able to deduce the disordered function from the structures damaged by the lesion. These are classical syndromes that have contributed to our understanding of the functional neuroanatomy of the brain stem.  For Anatomy 530a you should be sufficiently familiar with sections of the midbrain to recognize the consequences of the lesions causing the syndromes of Weber and Benedikt. You do not need to be visually familiar with sections of the pons, but you are expected to know that the nuclei of VI and VII are dorsally located at a caudal level of the pons, and that descending motor fibres (corticospinal etc) pass through the ventral part of the pons. You must also understand the differences between upper and lower motor neuron lesions that affect the facial and other muscles.
   Pontine lesions that impair conjugate eye movements are important for clinical diagnosis and functional neuroanatomy, but there will be no specialized neuro-ophthalmological questions in the final exam.

Midbrain lesions

Weber's syndrome Benedikt's syndrome Parinaud's syndrome
Weber's syndrome lesion Benedikt's syndrome lesion Parinaud's syndrome lesion
Fibres of III.
Descending motor fibres in cerebral peduncle.
Fibres of III.
Descending motor fibres in cerebral peduncle.
Red nucleus and nearby cerebellothalamic fibres.
Pressure on superior colliculi, usually by a pineal tumour, is transmitted to pre-oculomotor nuclei in region of posterior commissure and periaqueductal region
Ipsilateral oculomotor palsy.
Contralateral hemiplegia.
Ipsilateral oculomotor palsy.
Contralateral hemiplegia.
Contralateral tremor.
(Tremor is usually attributed to interruption of cerebellothalamic fibres but it may be continuous, from involvement of pallidothalamic fibres rostral to the red nucleus.
Paralysis of upward gaze and convergence, often accompanied by other pupillary and eye movement abnormalities.
Various pre-oculomotor nuclei, concerned with vertical eye movements, are present in the affected region.

Pontine lesions

Millard-Gubler syndrome Raymond's syndrome Foville's syndrome
Millard-Gubler syndrome lesion Raymond's syndrome lesion Foville's syndrome lesion
Facial motor nucleus and fibres of VII.
Descending motor fibres (but most are ventral to the lesion).
Descending motor fibres.
Fibres of abducens nerve.
Abducens nucleus.
Facial motor nucleus.
Ipsilateral lower motor neuron facial paralysis.
Contralateral upper motor weakness of limbs (which recovers with time).
Contralateral hemiplegia.
Ipsilateral VI nerve palsy (but no abnormality of movements of contralateral eye).
Ipsilateral VI nerve palsy and inability of the contralateral eye to adduct when attempting a conjugate movement. The contralateral eye does adduct with convergence to look at a near object.
Ipsilateral lower motor neuron facial paralysis.

Accounts of these syndromes were published between 1855 and 1895. The earlier investigators such as Millard and Foville had little understanding of the neuroanatomy. In the later studies, such as those of Raymond and Wallenberg, great efforts were made to fit the clinical findings to tracts and cranial nerve nuclei. The notion of the neuron as a cell and physiological unit, in its infancy in 1895, was finally proved in the 1950s. The notion of chains of neurons, linked by synapses, resulted from the work of Sir Charles Sherrington and other neurophysiologists who worked in the first half of the 20th century.

Acoustic neuroma. The effects of this benign tumour are presented in the lecture as a diagnostic exercise. The glial cells (Schwann cells) of the vestibular nerve proliferate and the resulting mass presses on the cochlear nerve, causing deafness. This happens where the two divisions of cranial nerve VIII are side by side and surrounded by bone, in the internal auditory meatus. The facial nerve is also present in this bony canal, and it is compressed. The tumour expands out of the internal meatus into the subarachnoid space, in the angle formed by the pons, medulla and cerebellum. As the tumour gets bigger it hits the side of the medulla (spinal trigeminal tract), and expands upward (roots of V) and downward (rootlets of IX, X). Click here to view a graphics file (acnroma2.gif) that relates the clinical features of an acoustic neuroma to the cranial nerves involved.
Test yourself. Why does this tumour, expanding into the pontocerebellar angle, spare cranial nerves VI and XII?   What structures other than cranial nerve roots might be pressed upon by a tumour in the pontocerebellar angle? (The tumour is benign only in the pathological sense of not being malignant. It will kill the patient if it goes on growing. How?)

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Last updated: 13th November 2007



























Sample questions

These multiple choice and short-answer questions test the subject in greater detail than is currently required for Anatomy 530a.
Don't expect to be able to answer all of them!
Neuro Quiz.  A collection of about 300 questions, grouped by subject. Answer by typing a word or short phrase. The correct answer is then shown and explained. All the files from the NEUROQUIZ.ZIP archive must reside in the same directory. The command  BQ  starts the program. For more information read the text file BQ.DOC

Download NEUROQIZ.ZIP (341055 bytes)

Neuro-MCQ.  About 140 multiple choice questions in Neuroanatomy. They can be chosen in groups by subject or at random from the whole collection. A single file, NMCQ.EXE, is all that is needed to run this program.

Download NEUROMCQ.ZIP (31043 bytes)

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