0 module

MBChB Phase 1
S6
Nervous System Module
Student Workbook
2020 - 2021
UNIVERSITY OF
DUHOK
COLLEGE OF MEDICINE

I
PREFACE
Content
Index:
Module Aims:
Self-study in anatomy:
Structure of the Module:
Videos and other electronic materials:
Related Modules:
Small Groups – Room Allocations:
Assessments:
Notes and Advices:
Staff of the module:
References:

II
Index:
SESSION ONE: Introduction to Structure and Development of Nervous System.
SELF STUDY ONE: The Internal Structure of the Brain and Spinal Cord.
SESSION TWO: The Environment of the CNS.
SESSION THREE: Somatic Sensation & the SensoryPathways.
SESSION FOUR: The Motor System
SELF STUDY TWO: The Skull and Cranial Nerves.
SESSION FIVE: Motor Disorders & Review of Patterns of Sensory Deficits.
SESSION SIX: Pain.
SELF STUDY THREE: Imaging & Neurophysiologic testing of Nervous System.
SESSION SEVEN: Neurotransmission & Its Clinical Correlates
SESSION EIGHT: Special Sense Organs – The Eye and the Ear.
SESSION NINE: Strokes, Head Trauma & CNS Imaging.
SELF STUDY FOUR: Special Senses and Higher Centres of the Brain.
SESSION TEN: Formative assessment and Neuroradiology
SESSION ELEVEN: Consciousness and Its Disturbances
SESSION TWELVE: Higher Functions of the Brain
SESSION THIRTEEN: Integration & Pathology
SESSION FOURTEEN: Formative assessment
Module Aims:
The aim of this module is to allow the student to develop a 3D concept of the system. Such a
concept is basic to the understanding and elucidation of clinical problems. You can
accomplish this task mainly by a study of the structure and function of the nervous system.
Self-Study:
Because of the shortage of material and limited teaching time not all necessary topics are
covered in these teaching courses. Therefore, you must seek such topics and some are
covered by self-directed sessions. Four Self Study Sessions are described in the workbook.
These require you to look at demonstration and other material designed to broaden your
general knowledge. So, the workbook sessions should be reinforced by private study.

III
Structure of the Module:
The module covers the physiology, applied anatomy of the nervous system, neurology and
related pathology and radiology.
The work is divided broadly into five sections covering:
a) the peripheral nervous system
b) the central nervous system
c) the cranial nerves and special senses
d) the environment of the brain and
e) Clinical Examination skills
The clinical aspects of these divisions are summarised by clinical presentation and the
analysis of case studies.
Videos and other electronic materials:
A lot of educational materials, other than the traditional lectures, will be available for you to
get use of and these could be obtained from the Moodle, Lecturers, Library and Medical
Education Unit.
Related Modules:
All the previous modules you had already received are so vital for comprehensive
understanding of this module, so please consult such modules as needed.
Small Groups – Room Allocations:
The names of the small group rooms and students allocation there are just like that in
Semester 5. If any change occur, you will be notify ahead.
Assessments:
You will be graded on the basis of attendance, participation at the small group and formative
assessments and upon summative assessment. Two formative assessments will be
arranged; at sessions 7 and 14 of this module.

IV
Notes and advices:
 We expect you to take full advantage of the opportunities the module provides.
 In addition to attending all the time-tabled sessions.
 You should read more broadly around the subject and use the follow-up questions in
the workbook and Moodle to guide that study.
 You may be asked to show us your workbook at any time as well as your specimen
correct answers to the questions in the workbook may be shown to you asneeded.
Staff of the Module:
Module Leader: Dr. Qasim Hasso
(qasim.hasso@uod.ac )
Dept of Physiology (Neurophysiology)
Co-Leader: Dr. Redir T. Hassan
(redir.hassan@uod.ac )
Dept of Anatomy (Neuroanatomy)
Lecturers: Dr. Qasim Hasso Dept of Physiology (Neurophysiology)
Dr. Sohaib Hasan Dept of Surgery (Radiology)
Dr. Dilshad Khorsheed Dept of Medicine (Neurology)
Dr. Nour Muafaq Dept of Surgery (Ophthalmology)
Dr. Abdulla Rabeea Dept of Surgery (ENT)
Dr. Mohammed Aziz Dept of medicine (Neurology)
Dr. Saleem Khadir Dept of Surgery (Radiology)
Dr. Kareem Mohammed Dept of Anatomy (Neuroanatomy)
Dr. Loqman Ismail Abdulla Dept of Anatomy (Neuroanatomy)
Dr. Redir Tahsin Hassan Dept of Anatomy (Neuroanatomy)
Dr. Perjan Hashim Taha Dept of medicine (psychiatrist)
Dr. Reveng Abdullah Dept of Physiology & Pharmacology
Tutors: All team (alternatively)
Dissection Room Educators: Anatomy team, neurosurgeons and other seniors
Clinical Educators: All team (alternatively) in addition to many specialist physicians
and seniors in relative specialties as needed

V
References:
Generally, below are the references and books that you may find particularly useful.
Additionally, you could consult relevant chapters in your textbooks or ask senior lecturers.
Author Title Publication Office
Carpenter R and Reddi B Neurophysiology Hodder Arnold
Fitzgerald, Gruener & Mtui Clinical neuroanatomy & neuroscience Elsevier
Siegel & Sapru Essential Neuroscience Lippincott,W & W
Crossman & Neary Neuroanatomy Churchill Livingstone
Krebs, Weinberg & Akesson Illustrated Revies Neuroscience Lippincott W & W
Young, Young & Tolbert Basic Clinical Neuroscience. Lippincott,W & W
Renton Medical Imaging Churchill Livingstone
General Physiology:
Vander, Sherman & Luciano Human Physiology McGraw Hill
Guyton & Hall Medical Physiology Sauders
Berne & Levy Principles of Physiology Mosby
General Anatomy:
Thieme Atlas of Head and Neck
Moore & Agur Essential Clinical Anatomy Lippincott W & W
Ellis Clinical Anatomy Blackwell
Snell Clinical Neuroanatomy Lippincott W & W
Anne Agur & Arthur Dalley Grant's atlas of anatomy Lippincott
Clinical Textbooks:
Kumar & Clarke Clinical Medicine Bailliere Tindall
Aminof clinical neurology Clinical neurology lipincotte
Davidson’s text book of medicine
Axford Medicine Blackwell
Clinical Examination
Douglas, Nicol & Robertson Macleod’s Clinical Examination Elservier, Churchill
Radiology
Armstong P & Martin W & Anderea R Armstrong's Diagnotci Imaging Willey-B.
Other useful books:
Goldberg Clinical Neuroanatomy Made Ridiculously Easy MedMaster, US
Pritchard & Alloway Medical Neuroscience Fence Creek
Bear, Connors & Paradiso Neuroscience Lippincott W & W
Diamond, Schiebel, Elson The Human Brain Colouring Book Harper Collins
Dissection guides and other neuroanatomical texts:
Chumbley & Hutchins A Colour Atlas of Human Dissection Wolfe
Jacobs Anatomy: A Dissection Manual & Atlas C. Livingstone
England & Wakely A Colour Atlas of the Brain & Spinal Cord Mosby
Internet, e books and other useful references and sites
http://www.doctorslongue.com
http://www.youtube.com/watch?v=vZBpNsFPJVQ
http://www.youtube.com/watch?v=jdaq-Ecz7Co
http://www.aclandanatomy.com

VI
Nervous System Module – Overview – S6
S.
N
o.
Da
te
Title 8.00 – 9.00 AM 9.00 – 10.00 AM 10.30 – 11.30 AM 12.00 AM – 2.00 PM
1
Module
Introduction:
Structure &
Developt of
the Nervous
System
Lecture 1: ……
Neurophysiology
Introduction to the
module & Self Study
Lecture 2: ......
Neuranatomy
Organisation of the
Nervous System
Lecture 3: ......
Embryology
Embryology of the CNS
Dissection Rooms:
...... Anatomy &
Relative Team
Gross Anatomy of N.
System
2
The
Environment
of the CNS
Lecture 1: ......
Neurophysiology
Cellular Physiology of
the Brain (Neurons &
Glial Cells)
Lecture 2......... Anatomy
The Environment of the
Brain (blood vessels,
meninges, skull and CSF)
Dissection Rooms .........Anatomy &
Relative Team
Gross Anatomy of the N. System
(Till 1.00 PM)
3
Somatic
Sensation,
Sensory
pathways &
Patterns of
Deficits
Lecture 1: ......
Neurophysiology
Somatic Sensation
The Ascending Tracts
Small Group Rooms ......... All Team
Patterns of Sensory Deficit
(Till 1.00 PM)
4
The Motor
System
Lecture 1: ......
Neurophysiology
Lower Motoneurons &
Muscle Stretch Reflex
Upper Motoneurons:
Descending Tracts
Lecture 3: ......
Neurology
Lesions of the motor
system
Small Group
dissection Rooms: ...
Relative Team
Review - Gross
Anatomy of NS.
5
Motor
Disorders
& Patterns of
motor Deficits
Lecture 1: ......
Neurophysiology
Physiology of Basal
Ganglia & Cerebellum
Lecture 2: ......
Neurology
Parkinson’s Disease
Small Group Rooms:...
All Team
Demonstrations on Upper
Motor Deficits and case
study
Small Group Rooms:
... All Team
Demonstrations on
Lower Motor Deficits
and case study
6 Pain
Lecture 1: ......
Neurophysiology
The Neural Basis of
Pain
Lecture 2: ......
Neurophysiology
Acute & Chronic Pain &
its Pathophysiol.
Lecture 3:... Clin.
pharmacology
Clinical Problem &
Analgesic Options
Small Group Rooms:
... All Team
Review
7
Neurotransmi
ssion & Its
Clinical
Correlates
Lecture 1......... Clin.
pharmacology
ChemicalDisturbances
of Neurotransmission
Lecture 2: ......
Neurology
Seizure Disorders &
Epilepsy
Small Group Rooms: ... All Team
Case studies on Disturbances of
Autonomic Function
(Till 1.00 PM)
8
Special
Sense
Organs The
Eye & The
Ear
Lecture 1: ......
Embryology
Embryology of the Eye
and the Ear
Lecture 2; ......
ophthalmology
The Eye & Central Visual
Pathways Cl. Disturb. of
Vision & Their Implications
Lecture 3 .........ENT
Mechanisms of Hearing &
their Pathologies
Small Group: ...
Related Team
Demonstration
9
Strokes;
Head Trauma
& CNS
Imaging
Lecture 1: ......
Neurosurgery
Blood Supply to the Brain
& Spinal Cord & Its
Disturbances (Strokes)
Lecture 2: ......
Neurosurgery
Head Trauma & Acute
Intracranial Events
Lecture 3: ......
Radiology
Neuroimaging
Small Group
Rooms: All Team
Case study and
demonstration
10
Neuroradiology,
Assessment & review
Formative
assessment – 1
(8.30 – 9.30)
Review
Lecture 1: ......
Radiology Neuroanatomy
Small Group
Rooms: Radiology
Team
11
Consciousne
ss
& Its
Disturbances
Lecture 1: ......
Neurophysiology
The Brainstem, Arousal,
Sleep & Origins of
Consciousness
Lecture 2: ......
Neurosurgery
Clinical Assessments of
Consciousness
Lecture 3: .......
Infectious Disease
Meningitis & Infectious
Diseases of the Brain
Small Group
Rooms: All Team
Review ... small
group session 10
12
Higher
Functions of
The Brain
Lecture 1: ......
Neurophysiology
Cortical Association
Areas
Lecture 2: ......
Psychiatry
Disturbances of Cortical
Function & Dementias
Small Group Rooms .........All Team
Case Study: Cortical dysfunction,
consc. & unconsc
(Till 1.00 PM)
13 Integration
Lecture 1: ......
Neurology
The Importance of History
Taking in the Diagnoses
of N S Disorders
Lecture 2: ......
Neurology
Examination of The
Nervous System
Lecture 3: pathology
Pathology of the Brain
Small Group Rooms
All Team
Review
14 Assessment & review
Formative
assessment - 2
Review
Dissection Rooms:
review
NS module team

1
Module introduction
Nervous system structure and development

2
NERVOUS SYSTEM - SESSION ONE
The Structure and Development of the Nervous System:
Aims:
 To give an overview of the nervous system, its peripheral and central
divisions and its role in the control of visceral and somaticfunction.
 To relate function in the nervous system to the anatomical
relationships and synaptic interactions between nerve cells.
 To discuss the emergent properties of neuronal interconnection and
the neurological problems associated with disruption of the nervous
system.
 To examine the external appearance of the brain and spinal cord.
 To outline the embryological development of the nervous system and
mention some problems of development.
Structure of the Session:
8.00-9.00 am Lecture 1: Introduction to Module
9.00-10.00 am Lecture 2: The Brain & Nervous System as anOrgan
10.30-11.30 am Lecture 3: Understanding CNS from its Embryology.
12.00-2.00 pm Dissecting Room: Gross Anatomy of the Nervous
System.
Readings: Siegel & Sapru (Chapt. 1,2,4), Crossman & Neary (Chapt. 1
& 2) and Ross (Nervous System Crash Course) Chapt. 1 & 2

3
Note:
Guidance On This Content: By the end of this Academic Unit, you
will have developed personalised ways in which to deal with the
Nervous System. At this stage of the course, all that is required is that
you familiarise yourselves with terminology on the structure and
varied ways in which the nervous system is described. This will slowly
make sense as the course progresses. Do Not Be Overwhelmed by
complexity of this subject.
Self Directed Study One: During the next two weeks you should
look at the demonstration material illustrating the internal structure
of the brain and spinal cord and do the work outlined in Self-Study
One. The material will be reviewed in Session Two

4
Session 1 – Lecture 1
INTRODUCTION
The building blocks of the nervous system are the neuron and the glial
cells. Neurons are responsible for the actions of the nervous systems
familiar to all of us. Glia, maintain an environment within which neurons
thrive. Thus, a healthy nervous system requires that both neurons and
glia are healthy.
As we already know from previous modules (e.g. Tissues of the body),
individual neurons can be very simple anatomically. Also, we now know a
great deal about them (e.g. Membranes and Receptors) even though
there is a lot more yet to be understood. Complexity in the nervous
system begins firstly, from the diversity with which neurons present in
terms of their anatomy, physiology, biochemistry, biophysics etc.
Secondly, when these neurons (bearing in mind their diversity) connect
to one another, the potential for complexity becomes even clearer. Some
connections, such as those of the monosynaptic stretch reflex are
relatively very simple, requiring only two neurons (hence monosynaptic).
This synapse (or connection between neurons) is highly favoured by
clinicians as it can be interrogated very easily and directly, thereby
revealing some information about the state of the nervous system. It is
also probably the cheapest form of diagnosis of the nervous system.
Commonly however, most connections between neurons not only involve
a lot of neurons but also chains of neurons, known as circuits, somewhat
analogous to common electrical circuits. Bearing in mind the billions of
neurons of the nervous system and their associated diversity, it becomes
clear that the trillion synapses they make between

5
them, form another basis for complexity of this system. At the extreme,
connections between neurons give rise to a series of emergent
properties, such as consciousness, thought processes etc.
When disruption occurs in such complex connections through injury or
degeneration, the nervous system can sometimes “make-up” for this
loss. In others cases, this will lead to deficits either in sensory, motor or
psychological function of the afflicted. As a clinician, you will be
examining the state of the nervous system throughout its hierarchy,
starting from the monosynaptic stretch reflex to assessments of moods,
thoughts and finally, consciousness. To be able to do this, you need a
good grounding on the basics of the nervous system. This module aims
to introduce you to some concepts of connections between neurons and
the functions of some well-known neuronal circuits.
To be effective in this module, we suggest that you prepare ahead of
each session by reading relevant material and make maximum use of
the scheduled teaching sessions. Additionally, self-directed study
sessions are to be approached as an integral part of the module.
Transcribing answers from friends and colleagues without understanding
how these were arrived at is not advised.

6
Session 1 - Lecture 2:
The Brain & Nervous System as an Organ:
Objectives: At the end of the introduction and with appropriate reading
you should appreciate:
 The central and peripheral divisions of the nervous system.
 The functions of afferent neurons and their relationship to sense
organs, efferent neurons in relation to muscles or glands and the
integrative properties of interneurons.
 The role of neuroglia.
 That the properties of the nervous system depends upon
interconnections between cells which are determined genetically and
modified by experience
 That an understanding of the pathways and connections within the
nervous system allows an approach to diagnosis.
 Some of the terms used to describe neurological disorder.
Lecture Synopsis: The nervous system is organised into the central
nervous system (CNS) and the peripheral nervous system (PNS).
The PNS is further divided into an
afferent (input) and an efferent
(output) division which again sub-
divides into the somatic nervous
system controlling skeletal muscle
and the autonomic nervous
systems regulating visceral
functions (see fig 1-1).

7
There are three classes of neurons a) afferent neurons which arise from
a sense organ and whose axons diverge in the CNS to come into contact
with many other neurons, b) efferent neurons, with a cell body located
within the CNS, upon which many other nerve cells converge and c)
interneurons - about 99% of all neurons - located entirely within the CNS
(some exceptions in the ANS) which integrate input with output. In
addition to neurons, the CNS contains large numbers of glial cells -
astrocytes, oligodendrocytes, ependymal cells and microglial cells, which
together make up about 90% of all cells and which support the neurons
structurally and metabolically. The CNS is very delicate, it is suspended
within the cerebro-spinal fluid, isolated from potentially harmful
metabolites in the blood by the blood-brain barrier, surrounded by three
meningeal layers and the whole protected within the skull and vertebral
column. It is highly metabolically active and will be irreversibly damaged
if its blood supply is interrupted for more than three or fourminutes.
The proper function of the nervous system depends upon anatomical and
synaptic links between neurons, which are determined both genetically
and by sensory experience. Malfunction occurs if either of these links is
disrupted. Analysis of malfunction depends upon an understanding of
neuroanatomy. In the PNS it is aided by the observation that sensory
input comes from clearly demarcated regions of the body - the
dermatomes, and that motor output affects distinct muscle groups - the
myotomes, and the finding that in the CNS specific function can be
localised within the brain

8
Fig:1:2 Localisation of Cortical Function: Brodmann Areas. Originally
the division of the cerebral cortex into numbered regions was based
upon histological differences. However some Brodmann areas are
synonymous with a specific function. Neurologists may refer to these
areas by number but more usually by function or location. NB this is not
a complete diagram
Area (Also
called)
Function Area (Also
called)
Function
3 (S1) Somatosensory cortex 4 (M1) Motor cortex
6 (PMA) Premotor cortex (area) 7 Sensory association
cortex
8 (SMA) Motor association areas 17 (V1) Visual cortex
41 (A1) Auditory cortex 45 Speech (Broca's
area)
Fig 1-2: Brodmann areas

9
Q1-1 Fig 1-3 is a diagram of the organisation of the PNS, showing
on the left fibers in the autonomic and on the right fibers in
the somatic nervous system.
Identify and label the structures indicated to show: (a) the
dorsal and (b) ventral roots, (c) a dorsal root ganglion, the
location of (d) an afferent nerve cell body, the location of an
efferent nerve cell body in (e) the autonomic and (f) somatic
systems, (g) a pre-ganglionic fiber and (h) the cell body of a
post ganglionic fiber of the autonomic system (i) an
autonomic ganglion. Is this ganglion in the sympathetic or
parasympathetic division of the autonomic NS?
Afferent Somatic Efferent
Afferent
Fig 1-3
Follow up Questions: Neurological disorders present with various
patterns of symptoms and signs. Some present an excess of some
feature e.g. increased muscle tone (hypertonia), or the emergence
of a new feature such as a tremor. Others show a loss or reduction
Visceral Efferent

10
of some function or ability e.g. muscle weakness (paresis), loss of
reflexes (areflexia), or changes in behaviour or personality.
The variety of signs necessitates a variety of descriptors. Many are
complex words containing a pre-fix e.g. a (without) combined with a
number of suffixes e.g. kinesis (movement) giving akinesis (without
movement) or with praxia (co-ordination) giving apraxia (lacking co-
ordination) etc.
The pre-fix a - means without - what is?
Q1-2 Akinesia
Q1-3 Apraxia
Q1-4 Agnosia
Q1-5 Aphasia
Q1-6 Areflexia
Q1-7 Ataxia
The pre-fix brady - means slow - what is?
Q1-8 Bradykinesia

11
The prefix dys - means disturbed what is?
Q1-9 Dysphagia
Q1-10 Dysarthria
Q1-11 Dysphonia
Q1-12 Dysdiadochokinesis
Q1-13 Dyslexia
The prefixes hyper - means too much - hypo - means too little
what is?
Q1 – 14 Hypertonia
Q1 – 15 Hyotonia
Q1 – 16 Paraplegia
Q1 – 17 Hemiplegia
Q1 – 18 Quadriplegia
Q1 – 19 Ophthalmoplegia

12
What is:
Q1 – 20 Paresis
Q1 – 21 Hemiparesis
Q1 – 22 Palsy
Q1 – 23 Chorea
Q1 – 24 Spastisity
Q1 – 25 Rigidity
This is far from a complete list, but these words will be part of
your medical vocabulary and you should add to them as you go
along

13
Readings:
 Langman's Medical Embryology
 Netter's Atlas of Human Embryology
 www.embryology.ch
Understanding the CNS from its Embryology
The embryology of the nervous system will be outlined with
emphasis on an explanation of how the complexity of the adult
anatomy arises. The lecture will cover the origin and fate of the
notochord, the development of neural folds and their fusion to create
the neural tube and the problems of failure of closure of the neural
pores. The differentiation and fate of neural crest cells will also be
covered along with the further development of the neural tube into
alar and basal plates that separate sensory and motor function. The
development of the spinal cord and the consequences of its
differential growth compared with that of the vertebral column. The
fusion of the neural folds in the cranial region will be outlined to
illustrate the eventual disposition of the five adult ventricles and the
relationship between cerebral hemispheres and brain stem.
Fig 1-5

14
Fig 1-4
Table 1-1 The relationship between foetal and adult anatomy
When describing features of the adult brain e.g. in the analysis of MRI images,
doctors use a mixture of terms. Some of these terms e.g. diencephalon /
midbrain / hindbrain etc. derive from the divisions of the embryonic brain,
others refer to regions of the adult brain e.g. cerebrum, brainstem still others to
individual features e.g. thalamus / pons / cerebellum etc.
The following table relates these approaches to the gross anatomy of the brain.
Embryologi
cal division
Telencephalon Diencepha
lon
Mesencephalo
n
Metencephal
on
Myelenc
ephalon
General
descriptions
Forebrain Midbrain Hindbrain
Regional
names
Cerebrum Diencepha
lon
Brainstem
Adult
features
Cerebral
hemispheres
Basal ganglia
etc.
Thalamus,
Hypothala
etc
Tectum &
tegmentum of
mid-brain
Pons,
Cerebellum
Medulla
Follow up Questions:
Q1-26 What is anencephaly? How does it arise?

15
Q1-27 What would be the consequences of a failure of the
neural fold to fuse in the lumbosacral region of spinal
cord? What is this condition called?
Q1-28 What conditions arises if (a) the meninges and (b) the
cord and meninges herniate through the unfused region
of the lumbar spine?
Q1-29 What condition arises if too much cerebrospinal fluid
accumulates in the vesicles of the brain?
Q1-30 How is this condition corrected after birth?

16
Session 1 – Dissecting Room:
Gross Anatomy of the Nervous System.
After this session you should understand a basic division of the CNS
into the forebrain (cerebrum & diencephalon), and the brainstem
(midbrain, pons, & medulla) and spinal cord.
You will be introduced to the salient features of the external
appearance of the brain and spinal cord. Indicate these, as
appropriate, on Figs. 1-6 and 1-7.
In the cerebrum identify:
The lobes and fissures of the cerebral hemispheres including the
longitudinal fissure, the lateral fissure, the frontal lobes, parietal
lobes, temporal lobes, occipital lobes.
Gyri & Sulci including the precentral gyrus, the postcentral gyrus,
the cingulate gyrus, the parahippocampal gyrus, the uncus. The
central sulcus, the calcerine sulcus and the parieto-occipital sulcus.
Commissural Fibers: corpus callosum, the anterior commissure.
Elements of the ventricular system: septum pellucidum, lateral
ventricle, third ventricle, the aqueduct, the fourth ventricle.
In the diencephalon identify: the thalamus. hypothalamus &
pituitary gland, the fornix, optic chiasm, the pineal gland.
In the brainstem: identify (from rostral to caudal) the midbrain with
the superior colliculi, inferior colliculi and the crus cerebri. The pons
and the medulla oblongata. Note the longitudinal striations running
through the pons and medulla. These are bundles of long
ascending and descending fibers passing through the brainstem

17
The cerebellum: note its divisions including the hemispheres,
vermis, tonsil etc.
Spinal cord: the meninges, the conus medullaris, the cranial and
lumbar enlargements of the spinal cord, the corda equina and filum
terminale, the lumbar cisterna. Note particularly the dorsal and
ventral roots, the cervical, brachial, lumbar and sacral plexi and their
relationship to the intervertebral discs and foramina of the vertebral
column.
Identify and label on
the diagrams:
the cerebral
hemispheres,
the frontal lobes,
the parietal lobes,
the temporal lobes,
the occipital lobes,
the cerebellum,
the medulla oblongata.
Gyri and sulci:
the precentral gyrus,
the postcentral gyrus,
the cingulate gyrus, the
lateral fissure the
central sulcus,
the calcarine sulcus, the
parieto-occipital sulcus.
Note
the pons,
Fig 1-6

18
the midbrain,
the diencephalon,
the thalamus,
the hypothalamus,
the superior colliculi, the
inferior colliculi,
the corpus callosum,
the fornix,
septum pellucidum,
lateral ventricle,
third ventricle,
aqueduct,
fourth ventricle. Fig 1-7

19
Identify and label on the diagrams:
olfactory tract
primary olfactory area
optic nerve
optic chiasm
optic tract
orbital gyrus
rectus gyrus
hypothalamus
uncus
insula
parahippocampal gyrus
medullary pyramids
occulomotor nerve
trochlear nerve
vagus nerve
pons
lateral sulcus
internal carotid artery
medulla cerebellum
Fig 1 - 8

20
Follow up Questions
To answer the following questions you should think about the
relationship between the spinal cord and the vertebral column.
Q1-31 Identify vertebrae L3 & L4 on a skeleton - why is thisan
important landmark when planning a lumbarpuncture?
Q1-32 Would you use a different landmark to perform alumbar
puncture in a baby? Why?
Q1-33 A vertebral fracture at T12 may paralyse the bladder. Why
is this, bearing in mind that the bladder is innervated by
nerves arising from spinal cord segments S2 - S4?
On the gross anatomy of the brain as shown in Fig 1 – 8:

21
Q1-34 What aspect of the brain is shown here?
Q1-35 Give 3 reasons why familiarity with this aspect of thebrain
is important.
Session 1 – Dissecting Room
The large group is divided into two main groups 1 & 2
Group 1 go to the Anatomy lab 1 and Group 2 go to the Anatomy lab 2. Each
Group should divide to appropriate small groups as needed (4-5 groups) and
Both Group should follow same instruction and subgrouping.
Note There are samples of teaching videos on the Moodle and
on CDs ... You should got them before this lab session.

23
NERVOUS SYSTEM - SELF DIRECTED STUDY ONE
The Internal Structures of the Brain and Spinal Cord
Introduction to the Self-Directed Study of the Internal Structures of
the Brain & Spinal Cord.
After this session you should understand:
 Basic neuroanatomical terms - anterior, posterior, rostral, caudal,
superior, dorsal, ventral, ipsilateral and contralateral with respect to
the nervous system as a whole.
 How grey & white matter are arranged in the spinal cord the cerebral
cortex and sub-cortical aspects of the brain.
 The meaning of the terms nucleus and tract as used in neuroanatomy
 The ascending and descending tracts and the anatomical basis of
conscious sensation and voluntary movement
Reading: Crossman & Neary (Anatomically relevant sections), other
references
Supportive materials: see the supportive materials provided along with
additional readings.
NOTE: Because the department cannot supply sufficient materials
for all students to complete this study at the same time, displays of the
relevant material will be available for self-directed study in the following
two weeks. The work is introduced in Session One and you should
complete it before the beginning of Session Two.
You will be looking at the supportive materials available as an aid to
the interpretation of these you should read, discuss and consult (if
needed).
Get use of the references, school web and other resources.

24
Synopsis: Nervous tissue consists of neurons and supporting glial cells.
Neurons have a cell body and axonal processes or nerve fibers . In the
brain and spinal cord, areas consisting mainly of cell bodies are referred
to as areas of grey matter, those consisting of nerve fibers as white
matter because of the myelination. In the brain, grey matter may exist as
an outer covering (in the case of the cortex) or as discrete areas inside
the brain. In sub-cortical structures of the brain, grey matter constitutes
nuclei. Examples will be presented of various regions of the CNS to
illustrate this point. Within the white matter nerves are collected into
bundles – i.e. tracts - which form pathways connecting different regions
of the CNS together. Each tract can be described anatomically
i.e. in terms of its connections and its course or pathway through the
system. They can also be described functionally e.g. as sensory or
motor tracts. Ascending tracts are sensory, bringing information from the
environment into the CNS where it may be consciously perceived, others
convey information about muscle length etc. which is not consciously
perceived. Descending tracts are motor, controlling movement, which
may be voluntary (conscious) or involuntary(unconscious)
Knowledge of the anatomy and the functions of these tracts and
nuclei is fundamental to neurological examination and the interpretation
of diagnostic images

25
Self Directed Study on the Internal Anatomy of the Brain & Spinal
Cord.
The Internal Anatomy of the Brain & Spinal Cord
1 Use the plastinated and model brains, and other materials, to revise
those features of the brain discussed in Session One.
2 Look at the dissected brains to see the insula, the corpus callosum,
the corona radiate, the caudate nucleus, and the lentiformnucleus
3 Look at brain Slices (coronal & horizontal section & other specimens):
identify and mark on appropriate diagrams: The cerebral cortex,
caudate nucleus, lentiform nucleus, corpus striatum, basal ganglia,
internal capsule, corpus callosum, lateral ventricle, third ventricle,
aqueduct, fourth ventricle, thalamus, (medial, anterior & lateral groups
of nuclei), hypothalmus, epithalmus (+pineal gland), cerebellum.
4 In models and sections of the brain stem recognise: midbrain, pons,
medulla oblongata by their shape and be able to name their important
features.
5 In plastinated or other specimens of the cerebellum: identify the
cerebellar peduncles, the deep nuclei, and cortex.
6 In models or photographs of the spinal cord: note the relationship
between the spinal cord, spinal nerves and the vertebrae. Note the
position of the functionally related substantia gelatinosa and the
periaqueductal grey matter.
HOW TO APPROACH NEUROANATOMY
BY THE END OF THE MODULE YOU SHOULD HAVE DEVELOPED IN YOUR MIND A 3D
MODEL OF THE CNS AGAINST WHICH NORMAL AND ABNORMAL FUNCTION CAN BE
JUDGED. AT THIS STAGE HOWEVER, ALL THAT IS REQUIRED IS THAT YOU BECOME
FAMILIAR WITH THE APPEARANCE, POSITION AND NAME OF THOSE PARTS OF THE
BRAIN WHOSE FUNCTION WILL BE REFERRED TO IN LATER SESSIONS.YOU
SHOULD NOT BE OVERWHELMED BY THE APPARENT COMPLEXITY OF THEBRAIN.

26
SD1-1 Look at 'Blue Slice' H-05.1 & H-05.2. identify the following
structures and indicate them on the diagram of a coronal section of the
brain:
The cortex The white matter The insula
The longitudinal fissure The lateral fissure The temporal lobe
The frontal/ parietal lobe The internal capsule The corpus callosum
The thalamus The hypothalamus The caudate nucleus
The lentiform nucleus The putamen The globus pallidus
The lateral ventricles The third ventricle The septum pellucidum
The hippocampus
Note: The Basal Ganglia:
A number of functionally related sub-cortical ganglia are known
collectively as the basal ganglia viz:
1.The Caudate Nucleus
Striatum
2.The Putamen The Basal Ganglia
The Lentiform Nucleus
3.The Globus Pallidus

27
SD1-2 Look for the following structures on 'Blue slice' H-05.11, 12 & 13
and
indicate them on the horizontal section of the brain:
The frontal lobes The temporal lobes The occipital lobes
The longitudinal fissure The lateral fissure The insula
The cortex The white matter The corpus callosum
The anterior limb of the
internal capsule
The posterior limb of the
internal capsule
The thalamus
The caudate nucleus The lentiform nucleus The globus pallidus
The putamen The third ventricle The lateral ventricles

28
SD1-3 Note the relationship between the cerebellum and the rest of the
brain in slice and identify the following structures marking them on this
diagram of a transverse section of the cerebellum:
The mid-brain The dentate nucleus The vermis
The cerebellar peduncles The fourth ventricle The cerebellar cortex
The white matter
See also the cerebellar peduncles in the dissection slices and diagrams

29
SD1-4 On the diagram of the brainstem Indicate the mid-brain, pons and
medulla and on the horizontal sections of each of these levels identify:
The fourth ventricle The aqueduct The medial lemniscus
The pyramids The inferior olivary nucleus The superior, middle &
inferior cerebellar
peduncles
The basilar part of the pons The tegmental part of the
pons
The corticospinal tracts
The cerebral peduncle The substantia nigra The red nucleus
The tectum The tegmentum The periaqueductal GM
The reticular formation

30
SD1-5 On sections of the spinal cord identify:
a) The dorsal horn b) The ventral horn
Familiarise yourself with the variations of the 'butterfly' shape of the
grey matter at various regions of the spinal cord
A
What level of the spinal cord
is illustrated in A
Indicate on fig B
B
1) The area where cells of the
substantia gelatinosa may be
found?
2) Where cell bodies of
sympathetic efferent fibers will
be situated
C
What level of the spinal cord
is illustrated in C

31
SD 1-6 At what levels in the cord will sympathetic efferent neurons be
found?
In diagrams and models note the relationship between the spinal cord
and the vertebral column.
SD 1-7 What vertebral level corresponds to the caudal end of theadult
spinal cord?
Look at sections of the vertebral column and notice the relationship
between the spinal cord the dorsal root ganglia, the spinal nerves and
the vertebral column.

32
Environment of the Nervous system

33
NERVOUS SYSTEM - SESSION TWO:
The Neuron & Environment of the CNS
Aims:
 To consider selected features of the anatomy of the skull.
 To consider the origin and circulation of the cerebrospinal fluid.
 To look at the blood supply to the brain.
 To look at the meninges of the brain & spinal cord.
 To consider clinical consequences of intracranial disease andhead
injury.
 To consider how the proper function of the nervous systemdepends
on its anatomical and biochemical integrity.
 To review previously covered material on Gross Anatomy of the Brain
& spinal Cord.
8.00 – 9.00 Lecture 1: Cellular physiology
9.00 – 10.00 Lecture 2: The Meninges, ventricles, CSF & blood supply
10.30 – 1.00 Dissecting Room: Gross anatomy of the brain.
Reading: Crossman & Neary (Chap 2) & Moore & Agur (Section 7 491-514).
Guidance on Content: This Session is delivered using the Round-Robin format.
There are 4 independent topics in this session. This session delivers more
information than can ever absorb at once. Treat the material covered here as an
Introduction to the topic in question. Most material from this session will be visited
more fully in later sessions. Set limits on information you wish to learn at this stage.
NO NEED TO PANIC!

34
Session 2 – Lecture 1:
Distinctive Features of the Neuron & CNS
Detailed learning outcomes
Following this lecture & with appropriate self-study you should be able to:
 Name the types of glial cells found in the central nervous system
and describe their roles.
 Describe the structure and function of the blood brain barrier.
 Describe the general morphology of a neuron and how
neurotransmitters are released.
 Name the major excitatory and inhibitory neurotransmitters in the
central nervous system and describe their action at receptors.
 Name the major amine neurotransmitters, understand that they are
located in discrete pathways, are implicated in various CNS
disorders and are major targets for CNS drugs.
Synopsis: This lecture serves as an introduction to the cellular anatomy
and biochemistry of neurons and glia in the central nervous system. We
will study how neurons and glia interact, what their functions are and how
neurons interact with each other. It will build on the work you have
already done in Tissues of the Body and Membranes and Receptors and
you should revise the relevant sections of these modules. You will find
the introduction to neurotransmitters useful for sections of the Clinical
Pharmacology module such as Parkinson’s disease, schizophrenia and
mood disorders.
The broad learning outcome of the nervous system module which this
maps to is: Explain how the proper function of the nervous system
depends on its anatomical and biochemical integrity.

35
Session 2 - Lecture 2
Environment of the brain
By the end of this lecture you should be able to:
 Outline the blood supply to the brain and describe the location ofthe
cranial dural sinuses.
 Describe the meninges and explain how they protect the brain.
 Describe the location of the ventricles in the brain, and outlinethe
formation, functions and circulation of cerebrospinal fluid.
 Name features of the skull and appreciate the importance ofcertain
skull injuries.
The Blood Supply to the Brain.
The blood supply to the brain comes from a matrix of blood vessels
derived from the internal carotid and vertebral arteries. The internal
carotid arteries enter the skull though the carotid canal and branch to
give anterior cerebral arteries supplying the medial surfaces of the frontal
and parietal lobes and the middle cerebral arteries, which supply the
lateral surfaces of the cerebral cortex. On entering the skull through the
foramen magnum, the vertebral arteries join to form the basilar artery
which supplies the cerebellum and brainstem. It then splits to give the
paired posterior cerebral arteries supplying the inferior surface of the
brain and the occipital lobes.
The cerebral arteries are joined together through the
communicating branches to form the circle of Willis at the base of the
brain. This anastomosis may provide a collateral circulation should one
of the arteries become progressively blocked, but is usually inadequate
following sudden occlusion of the cerebral vessels (cerebral thrombosis,
cerebral haemorrhage, cerebral embolism) and vascular stroke is a
common result.

36
The neuropil is drained by way of the cerebral veins and the venous
sinuses into the internal jugular vein. To enter the venous sinuses the
cerebral veins cross the subarachnoid space where they may be
ruptured e.g. following head trauma, leading to a subarachnoid
haemorrhage.
Q2-1 On these diagrams of the brain, colour and label those areas supplied
by the anterior, middle and posterior cerebral arteries.
Fig 2-1 Fig 2-2
Q2-2 What is the carotid sheath? Which structures lie inside it?
Q2-3 Which arteries supply the spinal cord?
Q2-4 What are the consequences of a blockage of a cerebral artery by an
embolus?
Q2-5 Define (i) vascular and (ii) haemorrhagic stroke
The main blood supply to the spinal cord is via the single anterior spinal
artery (ASA) and the two posterior spinal arteries (PSA).

37
Q2-6 What type of blood (arterial, venous, mixed) characterises
(1) Epidural (Extradural) haemorrhage
(2) Subdural haemorrhage
(3) Subarachnoid haemorrhage?
Q2-
7
Label on the diagram the arteries which form the circle of Willis:
Vertebral artery
Basilar artery
Posterior cerebral artery
Posterior communicating artery
Middle cerebral artery
Anterior cerebral artery
Anterior communicating artery
Q2-8 Which imaging procedure would be most useful indiagnosing
an aneurysm in a cerebral artery?
Fig 2-3

38
The Meninges:
The brain & spinal cord are covered by three meningeal membranes,
from outside inward the dura mater, the arachnoid mater and the pia
mater. The dura mater is a thick parchment-like membrane arranged as
an outer periosteal layer and an inner meningeal layer. The periosteal
layer is attached to the bones of the skull and vertebral column and
protects the brain and spinal cord by suspending them within their bony
casings. Extensions of the meningeal layer, the falx cerebri and the
tentorium cerebelli, stabilise the brain laterally and vertically.
The venous (dural) sinuses are spaces between the periosteal and
meningeal layers. These sinuses, including the inferior & superior
sagittal, straight and transverse sinuses link the venous drainage of the
brain into the internal jugular veins.
The arachnoid mater consists of a thin membrane attached to the
underside of the dura, and a web of tissue strands (trabeculae) which
not only attaches the meningeal dura to the pia mater but create a space
- the subarachnoid space which contains CSF.
The pia mater, the innermost layer is a delicate membrane that
tightly clings to the contours of the brain. The pial lining of the spinal
cord form the denticulate ligaments which secures the cord within the
spinal canal and at the caudal end of the spinal cord attaches it to the
dura through the filum terminale.

39
Following trauma to the head or haemorrhage within the skull,
pools of blood may form:
1 - between the skull and the periosteal layer of the dura - giving
an extradural (epidural) haematoma usually of arterial origin.
2 - between the meningeal layer of the dura and the arachnoid
mater - giving a subdural haematoma usually of venous origin.
3 - within the subarachnoid space - a subarachnoid haematoma
usually due to the rupture of an aneurysm of one of the vessels of the
arterial circle.
Rupture of the meninges in head trauma may allow CSF to escape.
Q2-9 Identify a to g on the diagram
a
b
c
d
e
f
g

40
The Skull:
The mechanical properties of the skull embedded in soft tissue will be
discussed in relation to applied forces. Delicate facial bones for example
the orbit, zygoma and the mandible, fracture easily. More severe trauma
gives rise to three classes of fracture related to the degree to which the
maxilla is detached from the skull (Le Forte fractures).
The energy absorbed during trauma may not result in fracture but
may still damage the brain causing oedema of, or bleeding into, the
cerebral substance. Fractures involving the vault of the skull may be
accompanied by disruption of dura & blood vessels leading to haematoma
formation between the arachnoid & dura or between the dura and skull.
The dura lining the 'base of the skull' is strongly adherent to the
periosteum. Fractures of this region can therefore result in dural tears
through which CSF can leak (rhinorrhœa & otorrhœa) and organisms enter.
Whereas vault fractures show up on skull X-ray, the skull base is not only
more dense but it’s left & right sides are always superimposed. CT is
usually required.
CSF rhinorrhoea is an example of an important consequence of a
fracture at a specific site, in this case a fracture involving the frontal sinus
or the cribriform plate in the anterior fossa. In the middle cranial fossa
fractures in the vicinity of the pterion may disrupt the middle meningeal
artery. Serious arterial bleeding from the nose results from tearing the
internal carotid artery as well as fracture of the body of the sphenoid.
Emergent cranial nerves can be involved e.g. loss of hearing in fracture of
the petrous temporal. The posterior cranial fossa is usually only fractured
when the mass of the body is decelerated against it and damage to the
brainstem means that few victims survive. The jugular foramen may be
disrupted & survivors suffer problems related to cranial nerves IX, X & XI.

41
Q2-10 On the diagram circle the position of the pterion and plot thecourse
of the middle meningeal artery

42
The Ventricles & Cerebrospinal Fluid (CSF).
The demonstration will look at the anatomy and relations of the four
ventricles of the brain with particular emphasis on how they may be used
to determine the plane of medical images, and how distortion or
expansion may indicate intracranial problems.
The production of CSF by the choroid plexus, its circulation
through the ventricular system and subarachnoid spaces and its re-
uptake, by way of arachnoid granulations, into the venous sinuses will be
outlined. Problems that lead to an excess CSF in the cranium are
defined in terms of communicating and non-communicating
hydrocephalus with or without a rise in intracranial pressure.
The properties of the CSF to provide protection for the brain, as a
medium through which the brain in nourished and how the chemical
integrity of the nervous tissue maintained will be discussed. Reference
will be made to the blood-CSF and the blood-brain barriers and how the
existence of these barriers may complicate the treatment of intracranial
infection etc. and how cerebral oedema may follow their disruption.
Trauma leading to leaks of CSF through the nose (CSF rhinorrhoea) or
ear (CSF otorrhoea) is referred to in other demonstrations (see Meninges
and Skull demonstrations)
The composition of CSF, how samples may be obtained, and how
changes in its composition can be a useful diagnostic tool will be
covered.

43
Q2-11 What is the composition of cerebrospinal fluid?
Q2-12 How and where is it produced?
Q2-13 Where is it reabsorbed?
Q2-14 Concerning hydrocephalus, what is
a) a communicating hydrocephalus?
b) a non-communicating hydrocephalus?
=============================
Session 2 – Dissecting Room
Group 1 go to the Anatomy lab 1 and Group 2 go to the Anatomy lab 2. Each
Group should divide to appropriate small groups as needed (4-5 groups) and Both
Group should follow same instruction and subgrouping.
Note There are samples of teaching videos on the Moodle and
on CDs ... You should got them before this lab session.

44
Somatic sensation and sensory pathways

45
NERVOUS SYSTEM – SESSION THREE
Somatic Sensation and the Sensory Pathway
Aims:
 To discuss the general properties of sense organs, the nature of the
transduction process and the encoding of the afferent input.
 To consider the ascending pathways of the spinal cord and their
central projection to the somatosensory cortex referring to their
somatotopic organisation at all levels.
 To consider sensory deficits associated with lesions in the sensory
pathways.
8.00-9.00 am Lecture 1: Somatic Sensation.
9.00-10.00 am Lecture 2: The Ascending Tracts.
10.30-1.00 pm Small Group Work: Patterns of Sensory Deficit.
Reading: Crossman & Neary (Chapt. 8), Berne & Levy (Chapt. 7),
Vander et al. (Chapt 9 & pp 223 – 240) & Siegel & Sapru (Section III,
Chapt 8: Section IV Chapt. 14)
Guidance on Content: Somatic Sensation is a specialty in its own right. It is a very
complex subject. At this stage of your training, you are not expected to know all the
intricacies of this subject. Instead we want you to have background knowledge on the
simplest neuroanatomical pathways that convey somatic sensation to the brain. You
are expected to know the simple rules of anatomy followed by the various anatomical
pathways. Please consult the learning outcomes above to guide you as to the scope
of this session’s content. This Workbook is particularly helpful in defining most of
what you are expected to know on this topic at this stage of your training. Its cases
studies were devised with students in mind.

46
Somatic Sensation:
At the end of this lecture and with appropriate reading you should
understand:
 The properties of receptor cells, the nature of the transduction process
and of receptor adaptation.
 How information about the nature, localisation and intensity of the
sensory input reaches the CNS.
 The receptive field of spinal afferent fibers and their somatotopic
distribution within the spinal cord and the somatosensory cortex.
 With reference to cutaneous receptors you should understand the
effect of the distribution of sensory endings upon tactile
discrimination.
Lecture Synopsis. Afferent neurons have receptors at their peripheral
endings which continuously inform the CNS of the conditions within the
external or internal environment. A receptor may be the bare terminal of
the afferent neuron, or a specialised structure at the nerve ending e.g. a
Pacinian corpuscle or it may be a separate receptor cell such as a rod
cell in the eye, which makes synaptic connection with the afferent nerve.
These receptors generate action potentials which are conducted to the
CNS. Afferent information may a) enter consciousness to give rise to our
perception of the world around us b) lead to an efferent output altering
motor behaviour, c) change our state of arousal (see Session 10), and/or
d) may be stored in memory for future reference.

47
Sensory Modality: We are responsive to a variety of stimuli - the
stimulus modalities - e.g. heat, light, chemical change, mechanical
pressure etc. Receptors respond preferentially to one modality, although
exceptionally they may be activated by others. The eye responds
preferentially to light although with a blow to the head, a, mechanical
stimulus, - we may “see stars”. Sensation therefore is dependent upon
the type of receptor activated.
Sensory transduction: When a stimulus impinges upon a receptor, it
causes a change in its membrane potential which is proportional to
stimulus intensity. This change affects the action potential generating
regions of the nerve, to set off a series of action potentials, which encode
information about the intensity, and duration of the stimulus. As all
afferent nerves transmit information in the form of action potentials,
knowledge of the nature and location of the stimulus depends upon the
connections afferent nerve fibers make within the CNS.
Receptor adaptation: Some receptors - tonic receptors - respond
continuously to the presence of an adequate stimulus. Others - phasic
receptors - rapidly adapt so that the action potential frequency in the afferent
nerve decreases during a maintained stimulus. Such receptors are sensitive to
change in stimulus energy.
Sensory Acuity: Each sensory neuron responds to a stimulus only if the
stimulus falls within its receptive field. The size of the receptive field
varies with receptor density. E.g. we have very few touch receptors on
the trunk so each one has a large receptive field. On our finger tips
however, we have a high density of receptors with small receptive fields.
The smaller the receptive field in a region the higher our acuity i.e. our
ability to locate the stimulus accurately and to distinguish between two
closely applied stimuli (Two point discrimination). Acuity may be

48
Enhanced by the process of lateral inhibition. These differences in
receptor density are reflected in the topographical map of the primary
somatosensory cortex.
Fig 3 -1: Shows a
section of the brain in the
coronal plane at the level of
the Internal Capsule. Note the
tight packing and wide
distribution of axons carrying
sensory information as they
pass through the Internal
Capsule
Coding of Sensory Information:
Property of
Stimulus
Mechanism of Coding
Stimulus Modality Type of receptor stimulated and specific sensory
pathway to the brain
Rate of change Receptor adaptation
Location Size of receptive field - enhanced by lateral inhibition
and the projection to a particular area of the
somatosensory cortex
Intensity Frequency of action potentials and the number of
receptors activated

49
Q3-1 Over what parts of the body can touch stimuli be most accurately
localised and why?
Q3-2 Why are you not continuously aware of the touch of your clothing as
you sit still?
Q3-3 What is meant by a topographical representation?
Q3-4 Explain why following a superficial skin burn sensation maybe
retained, but is lost with a full thickness burn?
Clinical Note: Shingles. Herpes zoster, the virus which normally
causes chicken pox, infects neurons of the peripheral nervous system
particularly cells in the dorsal root ganglia. After an initial infection with
chicken pox the virus may remain dormant, often for many years, before it is
reactivated in some way to produce the condition known as shingles.
Shingles increases the sensitivity of dorsal root neurons triggering burning,
tingling sensations which are extremely painful, the skin becomes scaly and
then blisters. As the virus is usually restricted to only one or two dorsal root
ganglia, the body areas affected by shingles reflect the dermatomal
distribution of those dorsal roots.

50
Q3-5 Why do sensory connections from the hand occupy a large area of the
cortex compared with those from the much larger skin area of the
thigh?
Q3-6 On the diagram of a lateral view of the brain outline the
somatosensory area and indicate to scale those areas receiving
information from: a) the hand b) the face c) the thigh
Fig. 3-2 Lateral View of the Brain

51
The Ascending Tracts.
Aims:
At the end of this lecture and with appropriate reading you should be
able to:
 Name the ascending tracts associated with the somatic sensesi.e.
touch, pain, temperature and proprioception.
 Describe each tract according to the scheme used in the
accompanying table.
 Use your knowledge of the ascending tracts to understand thesensory
effects of lesions in the CNS.
Lecture Synopsis: Sensory stimuli in the environment generate afferent
impulses in peripheral sensory nerves, which are transmitted into the
spinal cord or brainstem. Touch, pain, temperature and proprioception
(position sense) are the general or somatic senses, sight, hearing, taste
and smell are the special senses.
With the exception of some forms of proprioception, the somatic
senses are perceived consciously. For this to take place information has
to pass beyond the spinal cord or brainstem to reach the “highest” level
of the brain, the cerebral cortex. Unconscious proprioception is a function
of sub-cortical structures.
The ascending tracts are the pathways through which impulses are
passed from neuron to neuron until they reach the cortex. The
successive neurons are referred to as a first order neuron, second order
neuron etc. Each tract carries a specific sensory modality e.g. the

52
dorsal columns convey information about fine touch and proprioception.
As they ascend most tracts cross (decussate) from one side of the CNS
to the other, so that each side of the body sends sensory information to
the opposite (contralateral) side of the brain. The destination of the
ascending tracts for conscious sensations is the postcentral gyrus - the
primary sensory cortex or somatosensory cortex - in the parietal lobe. On
the way to the cortex most ascending tracts (there are some exceptions)
pass through the thalamus.
In this lecture emphasis will be placed upon the pathways of
conscious sensation. Each somatic sensory tract will be described,
following the scheme outlined in Table 3-1. The consequences of an
interruption of the ascending tracts by trauma or disease will be
discussed in following sessions.
Table 3-1. Sensory Pathways from the trunk and limbs
Tract Function Cell
bodies of
1st order
neurons
Cell
bodies of
2nd order
neurons
Cell
bodies of
3rd order
neurons
Decussati
on
Terminati
on
Pathways of Conscious Sensation
Dorsal
column -
Medial
lemniscal
Fine touch
Conscious
proprioceptio
n
Dorsal root
ganglion
Nucleus
gracilis or
Nucleus
cuneatus
Thalamus
Medulla Sensory
cortex
Lateral
Spinothalamic
Pain,
temperature
Dorsal root
ganglion
Dorsal
Horn
Thalamus Spinal
cord
Sensory
cortex
Anterior
Spinothalamic
Crude touch
Pressure
Dorsal root
ganglion
Dorsal
horn
Thalamus
Spinal
cord
Sensory
cortex
Pathways of Unconscious Sensation
Anterior &
Posterior
Spinocerebell
ar
Unconscious
proprioceptio
n
Dorsal root
ganglion
Spinal
grey matter
None Anterior in
spinal cord
Posterior
none
Cerebellu
m
Cuneocerebel
lar
Unconscious
proprioceptio
n
Dorsal root
ganglion
Nucleus
cuneatus
None None Cerebellu
m

53
The Sensory nerves of the face & head. (These nerves are also covered in
Session Eight)
Q3-7 How many neurons make up the conscious sensory pathway?
Q3-8 Why does some sensory input NOT reach consciousness?
The trigeminal nerve (Nv. V) is the major sensory nerve of the face and
head. Cutaneous information is conveyed from well demarcated areas of the face
by the ophthalmic, maxillary or mandibular division of the nerve (see Fig 3-3).
The cell bodies of the afferent nerves lie in the trigeminal ganglion and their
central processes synapse in the trigeminal nucleus in the brainstem. From there
second order afferent neurons ascend to the thalamus and third order neurons to
the cerebral cortex (see Fig 3-4).
Fig 3-3 Fig 3-4

54
Q3-9 What is sensory agnosia? Why might it affect a patient with a tumour
in the thalamus or internal capsule?
Q3-10 Identify the ascending tracts indicated on this TS of the spinal cord
and answer the questions related to each giving:
a) its name,
b) its modality e.g. conscious / unconscious proprioception, pain etc.
c) where it terminates,
d) where it crosses the CNS or none if it does not.
e) Origin of its 3rd order neuron - if it has one…..

55
Tract A
Name:
Modality:
Termination:
Site of Decussation:
3rd
Order Neuron:
Tract B
Name:
Modality:
Termination:
3rd
Order Neuron:
Tract C
Name:
Modality:
Termination:
3rd
Order Neuron:
Fig 3-5
ASCENDING TRACTS

56
Session 3 - Small Group Work:
Patterns of Sensory Deficit.
At the end of this session you should be able to
 Outline the sensory consequences of lesions in the ascending pathway.
In this session your tutor will discuss the consequences of various lesions of
the principal ascending tracts with reference to Fig. 3-6
Fill in the missing words:
1: A lesion at 1 affecting fibers in the...............................often follows a
…………………. The sensory losses will depend upon the extent of the damage but
can affect the whole body on the CONTRALATERAL / IPSILATERAL side
INCLUDING / EXCLUDING the face.
2: A lesion at 2 damages nerve cells in the............................... Again sensory losses
will depend upon the extent of the damage but can affect the whole body on the
CONTRALATERAL / IPSILATERAL side INCLUDING / EXCLUDING the face.
A lesion in the thalamus can also lead to a peculiar loss of awareness of the affected
side known as …………………
Fibers ascending in the dorsal columns cross over in the medulla (the arcuate fibers
) to form the medial lemniscus on each side of the brainstem. The anterolateral
spinothalamic fibers have already crossed over and ascend in the midbrain as the
spinal lemniscus.
3: Following a unilateral lesion of the brain stem at 3, sensation from the face will be
LOST / INTACT. Sensation in the limbs will be INTACT / IMPAIRED
IPSILATERALLY / IMPAIRED CONTRALATERALLY.
4: Transection of the spinal cord at 4 will lead to sensory losses which affect THE
WHOLE BODY / PARTS OF THE BODY below the lesion. ALL SENSATIONS /
ONLY LIGHT TOUCH & PAIN sensations will be impaired. The impairment will
involve THE CONTRALATERAL / THE IPSILATERAL / BOTH SIDES OF THE
BODY.
5: Destruction of a peripheral nerve supplying a limb e.g. at 5 will lead to the loss of
ALL SENSATIONS / ONLY SOME SENSATIONS and involve THE WHOLE LIMB / A
PARTICULAR DERMATOME.

57
Fig 3-6
Note: The extent of peripheral nerve sensory loss depends on the
diameter of the nerve transected e.g. a digital nerve cf. the sciatic nerve.
Furthermore, the area of sensory loss will shrink with time. Can you
explain?
Trige
Spin
Medi
lemn
Internal capsule Postcentral gyrus
Thalamus
1
2
minal
Midbrain
al
al
iscus
Trigeminal
nucleus
Trigeminal
nerve
Gracile
nucleus
Arcuate
fibers
Medial
lemniscus
Dorsal columns
Peripheral
nerve 5
3
Midpons
Medulla
SC cervical
level
SC lumbosacral
level
Anterolateral
Spinothalamic tract
4

58
Attempt these questions yourselves
Use information about dermatomal distribution you learned in the
Musculoskeletal Module to answer some of these questions.
Q3-11 Consider manikin1. Draw a line
on the tract diagram (mark it 1)
to show the site of a lesion that
would cause this pattern of
sensory loss.
1
Total sensory
loss
Q3-12 Specify the CNS or segmental
level of this lesion (e.g. pons,
C4, T6 etc.)
Q3-13 Consider manikin 2 and indicate
on the tract diagram (marking it
2) the site of a lesion which
would give this pattern of
sensory loss

59
2
C4, T6 etc.)
- by drawing a line (3) on the
tract diagram- the site of a
lesion giving this pattern of
sensory loss which has spared
the face. Show if your line is
confined to the IPSILATERAL
side /CONTRALATERAL side or
involves BOTH sides?
3

60
C4, T6 etc.)
on the tract diagram (4) the
likely site of a lesion that would
give this pattern of sensory loss
4

61
Peripheral neuropathy. A patient shows the
pattern of sensory loss shown in manikin 5 5
Q3-18
What is this pattern of sensory loss called?
Q3-19
Which neuron in the sensory pathway is damaged in this condition?
1st
ORDER NEURON
2nd
ORDER NEURON
3d
ORDER NEURON
Q3-20 What neuronal changes will lead to this pattern of sensory loss?
Q3-21 List some common disorders in which this pattern of sensory lossis
seen.

62
Nerve entrapment syndromes. In the Musculoskeletal Module you came
across some sensory losses e.g. carpal tunnel syndrome, sciatica etc. that
result from complete interruption of the affected nerve. However, patients
rarely present with such clear-cut patterns because only part of the nerve is
likely to be interrupted. Your patient presents with this pattern of sensory loss
Fig 3-7
Q3-22 What common entrapment
do you think this patient has?
Q3-23 Which nerve is affected?
Some lesions in the spinal cord may affect the ascending sensory pathway
on one side only. As fibers in the spinothalamic tracts cross over at the
segmental level, but those of the dorsal columns decussate in the medulla, a
differential sensory loss will be seen below the lesion.
Q3-24 Consider a lesion that partially
transects the spinal cord at T11
damaging ALL ascending fibers
on the RIGHT side of the cord.
Shade in on the manikin those
areas insensitive to somatic
(cutaneous) sensation and
those insensitive to pain.
(Remember that the cord is
bilaterally symmetrical)
Fig 3-7

63
Q3-25 What is this pattern of sensory loss called?
Some (rare) lesions selectively affect the dorsal roots and dorsal columns of
the spinal cord including:
1: Tabes dorsalis - the late symptoms of syphilis
2: Degeneration of the dorsal columns resulting from Vit B12 deficiency.
N.B. If you become a GP you should be acutely aware of this one as the
nervous degeneration will be seen even before any signs of anaemia
and the nerve damage can be put right with the injection of vitamin.
Q3-26 With these conditions what sensations will the patientlose?
Light touch / Conscious proprioception YES / NO
Pain / temperature YES / NO
Such patients will show a sensory ataxia and a positive Romberg sign
Q3-27 What is sensory ataxia?
Q3-28 What is a positive Romberg sign?
Your patient walks with difficulty picking his feet up and stamping them
down in the "stick and stamp" pattern of gait (See Fig 3-8)

64
Fig 3-8
Q3-29 Can you suggest what is wrong with him
and why he walks in this way? His
serum vit B12 is very low.
Q3-30 What is the general term used to describe
his condition?
Some (rare) lesions such as syringomyelia, selectively affect the
spinothalamic tracts of the spinal cord. This condition is due to the formation
of an elongated cavity or syrinx around the central canal of the cord. As it
expands it compresses fibers such as those of the spinothalamic tract which
cross segmentally in the mid-line of the cord.
Q3-31 With this condition what sensations will the patient lose?
Light touch / Conscious proprioception YES / NO
Pain / temperature YES / NO
Q3-32 Will the sensory loss be bilateral?
Q3-33 Why may a patient with this condition have scars and healing lesions
on his fingers?

65
RESUME
Anatomy of Sensory Pathways and Its Critical Role In Pinpointing
Site(s) of Lesion In The Clinical Examination of General Sensation
Knowledge of basic neuroanatomy of the sensory- and associated
ascending systems of the brain is essential if you are to carry out a
systematic and orderly clinical examination of the sensory system. It is
the only ‘tool’ that will allow you to gain insights on what sensory
modality is lesioned, where the lesion is likely to be located within the
hierarchy of the nervous system and how severe the condition is likely to
be. In specific cases, it might even allow you to guess what the
underlying/causative pathology is most likely to be. Taking the case of a
single spinal nerve root as an example, damage to this will produce
anaesthesia limited to its dermatome and no other symptoms. This is a
relatively minor lesion and sensation may return within a short time (say
3-6 months) as peripheral sensory nerves are capable of regeneration.
Severance of a complete nerve to a limb (e.g. the sciatic nerve),
however, will result in anaesthesia of the whole limb, spanning a
multitude of dermatomes. This will severely affect sensory function of the
limb in question, leading to possible damage to the tissues as protective
reflexes will have been eliminated (e.g. burns etc). Secondly, motor
function of that limb will also be heavily compromised since sensory
feedback, movement-induced sensory feedback (also known as
reafference), proprioception and kinaesthesia will no longer be available
to that limb. Vitamin B6 (also known as pyridoxine) poisoning or
advanced stages of syphilis infection can give rise to almost pure
sensory loss to the limbs. Traumatic damage to peripheral nerves is

66
unlikely to result in pure sensory loss since most of them are mixed and
can therefore be expected to include motor and autonomic loss to the
limb in question. In the case of a stroke or a major tumour in the highest
centres of the nervous system, sensation from an entire half of the body
may be compromised in isolation (e.g. capsular stroke or tumour). Given
this simple but exaggerated analysis, it is clear that, as a general rule,
there is a simple as well as direct correlation between the site and size of
a neurological lesion with severity of sensory deficit(s) resulting from
such a lesion. Lesions in peripheral nerves are likely to give rise to
limited areas of anaesthesia of the skin whilst lesions within the
substance of the brain have the potential to give rise to widely distributed
sensory deficits. Skilled history taking from a patient reporting a sensory
deficit is a necessary first step to determining the severity of the sensory
deficit whilst an orderly and systematic examination of the sensory
system will help you to confirm or even further delineate the severity of
compromise to sensation. Understanding the distribution and orderliness
of the hierarchy of the sensory system and experience in clinical
examination of the sensory system should help you to develop the skill in
predicting the general location of a lesion within the hierarchy of the
nervous system and to guess/predict with reasonable certainty the likely
effect such a lesion will have on the patient’s enjoyment of life. You are
likely to find this résumé very useful for the “History Taking” lecture
scheduled for Session 13.

68
NERVOUS SYSTEM: SESSION FOUR
The Motor System
Aims:
 To summarise the role of the cerebral motor cortex,cerebellum,
motor nuclei of the brainstem and spinal cord.
 To summarise the role of the spinal neural centres in motorreflexes
(stretch reflex).
 To cover the descending pathways of the spinal cord
 To contrast the consequences of lesions of the peripheral and
central nervous system in terms of changes in muscle power, tone,
co-ordination and reflexes.
 To outline the importance of clues to a disease process that can be
obtained from a detailed history.
8.00-9.00 Lecture 1: Lower Motoneurons & The Muscle Stretch Reflex
9.00-10.00 Lecture 2: Upper Motoneurons : Descending (motor) Tracts
10.30-11.30 Lecture 3: Lesions of The Motor System
12.00-2.00 Small Group rooms: lower and upper motor neurons ...
Reading: Crossman & Neary (Chapt.8, Chapt 11),
Berne & Levy (pp 111 – 133) & Vanderet al. (pp 340 – 350).

69
Muscle Receptors, Spinal Motor Nuclei and Spinal Reflexes
At the end of this lecture and with appropriate reading you should be
able to describe:
 The definition of lower motor neurons.
 The definition of a spinal reflex.
 The role of  &  motor neurons in the spinal cord.
 The properties and structure of muscle spindles & Golgi tendon organs.
 The postural and protective (stretch & flexor) reflexes and howthey
are tested.
 Describe the main descending tracts of the motor system.
Lecture Synopsis. In neurology, neurons constituting the motor system
are collectively known as motoneurons. These are further qualified into
upper or lower motoneuron categories depending on their location within
the hierarchy of the motor system. This terminology becomes invaluable
when motor disorders are to be classified. Damage to upper motoneurons
gives rise to a distinct constellation of presenting signs,
known as upper motoneuron signs.
Conversely, lower motoneuron pathologies
have their own unmistakable presenting
signs, lower motoneuron signs. In cases
where there are simultaneous pathologies
of the upper and lower motoneuron
systems, presenting signs become
indistinguishable from lower motoneurons
signs. In this lecture, lower motoneurons
Fig 4-1

70
will be introduced. By definition, lower motoneurons are those cells whose
cell bodies collect to form discrete motor nuclei of cranial nerves in the
brainstem or spinal nerves. Their axons form the crucial "final common
pathway" between the nervous system and all voluntary muscles of the
body. Lower motoneurons are the only neurons of the body that produce
movements through the activation of muscles. These movements can be
reflexive in response to segmental inputs or volitional as directed by
higher centers of the CNS acting via upper motoneurons. There are two
kinds of lower motoneurons, alpha (α) motor neurons and gamma ()
motor neurons. In this lecture we will introduce the concept of the lower
motoneuron, features of these two types of neurons, the muscle stretch
reflex and segmental reflexes and their importance in the examination of
the motor system. You are expected to supplement this lecture with
further reading in advance and to integrate it with your knowledge from
clinical examination skills of the nervous system. Fig 4-1 illustrates an
example of a spinal reflex circuit, the knee jerk. Others are given in Table
4-1.
Demonstration-Small Group Tutorial: (Muscle Stretch Reflexes)
The aim of this Demonstration-Tutorial is to formally introduce the basic
neuro-clinical skill of testing for limb tendon reflexes. Your Clinical
Demonstrator will use the knee-jerk as an example to demonstrate how
tendon reflexes are routinely elicited during neuro-examination. It is
fortuitous to introduce this skill in this session because your Clinical
Demonstrator will not only facilitate you to try eliciting reflexes on each
other but will also help you to attend to the small group work questions
below. Please make sure that by the end of this session, you understand
this subject and are very happy with the subtlety to some of the questions
below.

71
Q4-1 What is the strict definition of a reflex?
Q4-2 Reflex pathways are constituted from 5 genericanatomical
components. Please list these.
In the case of the muscle stretch reflex, please draw a fully
labelled diagram of this circuit, making sure you identify the
anatomical constituents of the reflex mentioned immediately
above
Q4-3 What do you understand by the term, “reflex movement”?
When examining movements in a patient, why is it important to
distinguish between voluntary movements and reflex
movements?
Q4-4 Give an example of a common class of limb motorreflexes
routinely examined as part of a medical examination

72
Q4-5 What is the relationship (or distinction) between a monosynaptic
stretch reflex and a muscle stretch reflex (also known as the
MSR)?
Q4-6 The term “muscle stretch reflex” is an umbrella term for a series
of motor reflexes that can be evoked following stretch of a
muscle. Identify the various sub-types of stretch reflexes.
Q4-7 When testing for tendon jerk reflexes in a healthy individual
exhibiting normal responses, which of the sub-types above (Q 4-
6) of the muscle stretch reflex is most likely elicited?
Q4-8 Apart for the muscle stretch reflex sub-type just identified in Q4-6
above, what is the explanation then for the failure to evoke the
other sub-types of muscle stretch reflexes when testing for limb
reflexes in a relaxed healthy individual exhibiting normal
responses?
Q4-9 It is to be expected that when testing muscle stretch reflexes in
some relaxed healthy individuals, they may be found to be
areflexic or severely hyporeflexic. What is the explanation for this
otherwise normal feature in such individuals?

73
Upper Motoneurons: Descending (motor) Tracts
Objectives: At the end of this lecture and with appropriate reading you
should be able to describe:
 The hierarchy and main components of the motorsystem
 The two main classes of descending tracts, their functionsand
general organization
 The distinction between upper and lower motoneurons
 The relationship bet we en the p yr amidal system and
lower motoneurons
 The relationship between the extra-pyramidal system andlower
motoneurons
 Differences between clinical signs subsequent to lesions ofthe
pyramidal system from those of the extra-pyramidal system
Lecture Synopsis. The neural apparatus that generates, executes,
maintains and terminates movements is known as the motor system. It
is hierarchically organized with motor areas of the cerebral cortex
highest, brainstem nuclei and the cerebellum intermediate and
motoneurons of cranial and spinal nerves lowest. Clinically, the motor
system is divided into 2 functional categories, upper and lower
motoneurons. Lower motoneurons are defined as cells of the ventral
horn of the spinal cord or cranial nerve motor nuclei that give rise to
axons that supply skeletal muscles. Upper motoneurons are defined as
neurons of the cerebral motor cortex and brainstem nuclei that in turn
connect with lower motoneurons. Upper motoneurons are themselves
further subdivided into pyramidal and extra-pyramidal

74
systems. The pyramidal system has direct (monosynaptic) contact with
lower motoneurons supplying distal muscles of extremities (e.g. hand)
whilst the extra-pyramidal system has an indirect contact with the rest of
the motoneuron pools. Lesions anywhere in the lower motoneuron will
produce flaccid paralysis (or atonia), atrophy, fasciculations and
hyporeflexia (if not areflexia) of muscles supplied by that motoneuron. In
contrast, lesions of upper motoneurons give rise to complex signs
depending upon whether the pyramidal or extra-pyramidal system is
affected. Typically however, they both produce spastic paralysis (or
increased muscle tone), minimal or no atrophy, no fasciculations, and
hypereflexia. A further sign indicative of lesions of the extra-pyramidal
system may include the generation of unwanted or uncontrollable
movements (chorea). In the case of the pyramidal system, a positive
Babinski sign will be seen following stroking of the lateral aspect of the
sole of the foot. This lecture will introduce you to the general
organization of the main descending systems and their roles in the
generation of movements.

75
Table 4-1 Pyramidal Motor Pathways
Tract Function Origin Decussation Termination
Lateral
Corticospinal
Tract
Voluntary
movement
Motor & premotor
cortex & precentral
gyrus
Medulla
(pyramidal
decussation)
Contralateral
spinal cord
Ventral
Corticospinal
tract
Voluntary
movement
Motor & premotor
cortex & precentral
gyrus
Spinal cord Contralateral
spinal cord
Corticobulbar Voluntary
movement
Motor & premotor
cortex & precentral
gyrus
Brainstem Contralateral
motor cranial
nerve nuclei
Extrapyramidal Motor Pathways
Tract Function Origin Decussation Termination
Tectospinal Turns head toward
sights or sounds
Tectum
(colliculi) of
brain
Brainstem Neck & upper
thoracic spinal
cord
Rubrospinal Flexor muscle tone Red nucleus Brainstem Neck & upper
thoracic spinal
cord
Reticulospinal Automatic
movement (e.g.
locomotion)
Reticular
Formation
Partially in
brainstem
Spinal cord
Vestibulospinal Balance & posture Vestibular
Nucleus
None Spinal cord
After the lecture you will need to read about the topography of the
spinal cord and its blood supply in your topography textbook and
neuroanatomy text.

76
Q4-10 Identify the descendingtracts indicated on this TS of the spinal
cord and answer the questions related to each giving:
a) its name,
b) its function e.g. voluntary / involuntary control of muscles,
c) where it crosses the CNS or none if it does not.
Tract A
Name:
Function
Site of decussation:
Tract B
Name:
Function
Tract C
Name:
Function
Tract D
Name:
Function
DESCENDING TRACTS
Fig 4-2

77
Lesions of the Motor System:
should be able to:
 Distinguish the differences and understand the consequences of a
"motor" lesion in the central and peripheral nervous systems.
 Outline cardinal signs indicative of lower motoneuron lesions(lower
motoneuron signs)
 Explain the underlying scientific basis to the emergence of lower
motoneuron signs
 Outline cardinal signs indicative of upper motoneuron lesions(upper
motoneuron signs)
 Distinguish between pyramidal & extra-pyramidal uppermotoneuron
signs
 Explain the underlying scientific basis to the emergence of lower
motoneuron signs
Lecture Synopsis: In neurology, being able to decipher the symptoms
and signs of where a lesion is situated, is of prime importance when
making a diagnosis and planning for treatment. The first important
distinction to be made is between so-called Upper Motor Neuron (UMN)
and Lower Motor Neuron (LMN) disorders placing the lesion in the
higher centres of the CNS or lower centres of the CNS or PNS.

78
7
Damage to the motor tracts of the brain and spinal cord are termed
Upper Motor Neuron Lesions to distinguish them from the Lower Motor
Neuron Lesions consequent upon damage to cranial or spinal motor
nuclei or peripheral nerves. Damage to the motor tracts in the brain
gives rise to either pyramidal or extrapyramidal signs. Pyramidal signs
are called upper motor neuron signs and arise from damage to the
corticospinal tract. These tracts travel from the motor cortex to the
anterior horn cells of the spinal cord and are sometimes referred to as
"long tracts". Extrapyramidal signs arise from damage to the
extrapyramidal tracts (Rubrospinal, Tectospinal, Vestibulospinal and
Reticulospinal tracts) and produce signs related to dysfunction of non-
cortical motor systems such as the basal ganglia and cerebellum.
The presence of other neurological signs along with long tract signs
can indicate the site of a lesion. Damage to the corticospinal tract
impairs the volition of fine movements. Damage to the extrapyramidal
tracts impairs the way movements are carried out (e.g. gait
abnormality).
The term ‘motor’ is used with respect to these disorders even
though sensory abnormalities, such as those we considered in Session
Two are often present as well. This lecture-demonstration will outline
the motor signs of peripheral and central lesions and differentiate them
in terms of their effects on muscle power and tone, co-ordination and
reflexes.
Note 1: Spinal Shock. A period of spinal shock follows when the descending tracts of the spinal cord are
severely damaged. This period, which may last for weeks or months, is characterised by a flaccid paralysis and
areflexia even though the ventral roots may be intact. Eventually the limbs become spastic and show hyperactive
deep reflexes, typical of upper motor neuron damage. The reasons for the loss of reflex activity in shock is
thought to involve the loss of motor influences exerted by descending fibers from the reticular formation. As these
fibers degenerate, the intact connections in the reflex circuits become dominant and show themselves
as upper motor neuron signs
Note 2: Muscular weakness can arise from conditions, which affect the muscles (myopathies), or the neuro-
muscular junction (e.g. myasthenia gravis). These conditions were covered in the Musculoskeletal module

79
Q4-11 List five signs that distinguish upper / lower motor neuron lesions
Upper motor neuron Lower motor neuron
1 1
2 2
3 3
4 4
5 5
Q4-12 Give three other associated features
1 1
2 2
3 3
The appearance of the sign of Babinski indicates an Upper Motor Neuron lesion.
Q4-13 What is the sign of Babinski?

80
RESUME
The Clinical Importance of the Motor Unit and the Stretch Reflex
In your own time and at your convenience, you will find it very beneficial
to use appropriate information to describe the following:
 The muscle stretch reflex
 The distinction between the muscle stretch reflex and the
monosynaptic stretch reflex
 The properties structure of muscle spindles
 The central connections of muscle spindle afferents
 The versatility of the muscle stretch reflex and its critical importance
in the construct and examination of spinal reflexes
 The definition of a spinal reflex.
 The role of  &  motor neurons in the spinal cord.
 The properties and structure of muscle spindles and Golgitendon
organs.
 The postural and protective (stretch
& flexor) reflexes and how they are
tested.
 Describe the main descending tracts
of the motor system

81
Testing muscle reflexes by brisk tapping of tendons is a common
procedure in examination of the motor system. Although such a test is
simple, requires only a tendon hammer and makes of use of a small
number of neurons connected together, the versatility of the muscle
stretch reflex is not to be under-estimated, first in terms of its
importance in the building of limb and postural reflexes. Secondly, when
it is used in the clinical examination of the nervous system, it reveals
unambiguously definitive information on the state of health of the
nervous system. Whilst this appears a very simple subject at first sight,
scientific principles underlying this circuit(s) and its derivatives are too
advanced and as such will not be tackled at this stage. However, those
with interest on this subject will find a vast body of published literature
at your disposal.
The afferent and efferent integrity of various
nerve roots are examined by testing reflexes
Table 4-2 Root values of tendon reflexes
Root Value Reflex
C 5-6 Supinator
C 5-6 Biceps
C 7 Triceps
L 3-4 Knee
S 1 Ankle

83
NERVOUS SYSTEM: SELF DIRECTED STUDY TWO
The Skull and Cranial Nerves. Dissecting Room
Group 1 go to the Anatomy lab 1 and Group 2 go to the Anatomy lab 2.
Each Group should divide to appropriate small groups as needed (4-5
groups) and Both Group should follow same instruction and subgrouping.
Aims: At the end of this session you should be able to:
 Identify the general features of the adult skull.
 Identify the anterior, middle and posterior cranial fossae and
appreciate their relationship to the contours of the base of thebrain.
 Identify named foramina of the skull base and specify the structures
that pass through them.
 Understand the differences between the adult and thefoetal/neonatal
skull and be aware of the growth processes that create them.
 Appreciate the articulation of the head and the structure andvariation
of the vertebrae.
 Identify the anatomical features of the inferior aspect of the brain.
 Identify the twelve cranial nerves.
In this session demonstration material will be available referring to
the skull, the vertebral column and the cranial nerves. You should
look at this material with reference to your anatomy textbooks.

84
The Skull.
Use your anatomy text books and other materials to identify the
following features of the skull, indicate these on all appropriate
diagrams.
External Features: Note the cranium (enclosing the brain) and the
facial skeleton
Find the landmarks:
Proceed in a sagittal direction: mental protuberance, nasion, glabella,
the bregma, the lambda, the external occipital protuberances
Proceed coronally: angle of mandible, zygomatic arch. the pterion, the
temporal lines.
Examine the Skull in more Detail:
Anterior Aspect:
Bones: Frontal bone*, Nasal and Zygomatic bones. The maxillae*. The
mandible with its body and ramus. The maxillary and mandibular teeth.
Sphenoid* & Ethmoid* bones (within the orbit of the eye).
*Visualise the sinuses within these bones.
Apertures: The orbits and the nasal aperture, nasal septum.
Fissures/Foramina: Orbital fissures, optic canals
Sutures: The sutures between the maxilla and the zygomatic, frontal and
nasal bones. (Note that they make a sort of triangle).
Lateral aspect:
Bones: Parietal. Temporal - identify its squamous and petrous
parts and its styloid and mastoid processes. Sphenoid. Occipital. Look at
the articulation of the jaw.

85
Apertures:External auditory meatus
Sutures: Coronal. Lambdoid. Parietotemporal. Squamoparietal. Note
the pterion at the junction of the parietal and sphenoid bones.
Posterior aspect:
Bones: Parietal and Occipital bones. Note the nuchal lines on the occipital
bone.
Sutures: Note the junction of the parietal and lambdoid sutures at the
lambda.
Inferior aspect:
Bones: Note that the base of the skull is made up of the occipital,
temporal, sphenoid bones and the maxilla which forms the hard palate.
Note the occipital condyles.
Apertures: Foramen magnum
Foramina: There are many "holes" in the base of the skull through
which blood vessels and cranial nerves pass. Note in particular the
carotid canals. The jugular foramen. The stylomastoid foramen.
Foramen lacertum. (For other foramen see p342 - 348 Moore & Agur).
Internal features: The cranial cavity is divided into the anterior, middle
and posterior fossa. Notice that the floor of the cranial cavity is quite
rough. Consider what effect this has upon the base of the brain if it is
caused to move within the cranium with for example a sudden
acceleration / deceleration.
Note the bones making up the floor and walls of each of the fossae.
In the anterior fossa notice the cribriform plate and the crista galli (the
anterior attachment of the falx).

In the middle fossa note the anterior and posterior clinoid processes
forming the corners of the sella turcica (the Turk's saddle) and
surrounding the pituitary fossa and the relationshipbetween
the
Pituitary and the optic tract. Note the grooves corresponding to the
middle meningeal artery (relate this to the pterion),
In the posterior fossa note the petrous
part of the temporal bone and the internal auditory aperture. Notice the
impressions in the bone of the transverse sinuses and the petrosal
sinus and of the cerebellum separated by the internal occipital crest.
Frontal aspect
Lateral aspect
86

87
External aspect of base
Internal aspect of base

88
SD2-1 Name the structures passing through:
a) the foramen ovale
b) the jugular foramen
c) the carotid canal
SD2-2 List all the
magnum
structures that pass through the foramen
The neonatal skull
Examine a neonatal skull. Notice
the large size of the cranium relative
to the face. The
posterior fontanelles.
sutures and compare
anterior and
Note the
them to the
sutures of the adult skull.
SD 2-3 What is the importance of
fontanelles and sutures during
childbirth?
Examine the display of bones and the radiographs of
compare the proportions of child and adult skulls.
skull growth to
Look also for
developmental changes in the teeth, the paranasal sinuses and the ear
region.

89
Foramina of the Skull
Look at the other X-ray material, which illustrates skull trauma and potted
prosections showing the cranial nerves leaving the skull through their
foramina.
The articulation of the head:
Look at an intact skeleton; note how the occipital condyles on the base
of the skull articulate with the articular facets of the atlas to form the
atlanto-occipital joint. Note also how the axis relates to the atlas.
Movements between the skull and the atlas are flexion and extension -
nodding - YES - movements. Movement between atlas and axis is
rotation - shaking the head - NO - movements.
The vertebral column
Identify the atlas (C1) and the axis (C2) vertebrae.
Examine the axis and identify the odontoid process. Articulate the axis
and the atlas and observe the articulation of the odontoid process with
a facet on the anterior arch of the atlas. Note also the joints between
the superior articular process of the axis and the inferior articular
processes of the atlas. The three articulations together form the atlanto-
axial joints.
On a disarticulated spine attempt to flex/extend the atlas on the axis.
Observe the odontoid process as it protrudes into the vertebral canal.

90
Look at a disarticulated vertebral column to identify: the cervical,
thoracic, lumbar vertebrae and the sacrum and coccyx. Note specific
features identifying each region, the intervertebral discs, the
articulations between the superior and inferior articular processes of
adjacent vertebrae, the relatively small intervertebral foramina easily
encroached upon by bony outgrowths from these articulations. (Use
information you have gained from the Musculoskeletal Module)
In particular note the relationship between the intervertebral discs in
relation to the vertebral canal and the intervertebral foramina
SD2-4 What would be the consequences of a postero-lateral
prolapse of an intervertebral disc?
SD2-5 Label this diagram of a vertebra to show a) the body, b) the
lamina, c) the pedicle, d) the spinous process, e) the
vertebral canal, f) the transverse process, g) the articular
processes.
Fig SD 2-6 A vertebra
SD2-6 On Fig SD 2-6 cross hatch the area of bone that would have
to be removed during a laminectomy to expose the cord and
roots on one side.
Fig1

91
SD2-7 From which region of the vertebral column does thisvertebra
come?
Look at a cervical vertebrae and identify the foramen transversarium.
Note that when all the cervical vertebrae are joined together, the
foramen join together to make a channel
SD2-8 Which artery runs through this channel?
In older people arthritic change in the joints between the articular
processes of the cervical vertebrae may partially occlude this channel.
The Cranial Nerves.
Examine a plastinated or model brain and using the illustrations and
other materials, identify: the olfactory bulb, the olfactory tract (Nv I) the
optic nerve (Nv II), the optic chiasma and the optic tract.
You should then identify the remaining ten cranial nerves: (You should
remember them by name & number)
III - oculomotor IV - trochlear V - trigeminal VI - abducens
VII - facial VIII - vestibulocochlear, IX – Glossopharyngeal
X - vagus XI - accessory XII – hypoglossal

92
SD2-9 As you identify the cranial nerves label them on the
following diagram. Indicate which are entirely motor (M)
which entirely sensory (S) and which are mixed (M/S)
Detail of Base of Brain

93
SD2-10 Look at the following brain slice:
Which cranial nerve nuclei are present in this brain
slice? State whether each of these is motor only
(M), sensory only (S) or mixed (M/S)

94
Motor and sensory disorders

95
Guidance on Content: This is a Review Session. Most of this
Session’s content should not be new to you. The Session is intended
to help you consolidate material from Somatic Sensation & Motor
System. Do Not Panic if some content appears new to you.
NERVOUS SYSTEM: SESSION FIVE:
Motor Disorders & Review of Patterns of Sensory Deficits.
Aims:
 To get consider the physiologic background of the basal ganglia and
cerebellum and their neuronal circuits.
 To consider the specific case of Parkinson disease as an example of a
CNS degenerative disease process that impairs the motorsystem
 To discuss the localization of a lesion with reference to the anatomy
and properties of the motor pathways
 To contrast the consequences of lesions of the peripheral and central
nervous system in terms of changes in muscle power, tone, co-
ordination and reflexes.
 To outline the importance of clues to a disease process that can be
obtained from a detailed history.
 To review case studies on Patterns of Sensory deficits
8.00-9.00 am Lecture 1: Physiology of Basal Ganglia & Cerebellum
9.00-10.00 am Lecture 2: Parkinson’s Disease
10.30-11.30 am Small Group: Demonstrations: Upper motor neuron dis.
12.00-2.00 pm Small Group: Demonstrations: Lower motor neuron dis.
Reading: Crossman & Neary (p86 - 87, p123, & p158 – 160)

96
Session 5 Lecture 1:
Physiology of the Basal Ganglia and Cerebellum
Objectives: After this lecture you should be able to:
1- Discuss the general role of the cerebellum and basal ganglia involuntary
movement
2- Describe the organization of the cerebellum
 List the major inputs/outputs to and from the cerebellum
 List the major functions of the three functional divisions of thecerebellum
3- Describe the organization of the basal ganglia
 List the major inputs/outputs to and from the basal ganglia and their
corresponding neurotransmitters
4- Trace the connections of both the direct and indirect pathway of the basal ganglia
and their contributions to movement
5- Relate how disorders of the basal ganglia such as Parkinson’s diseaseaffect
these pathways
Synopses: The basal ganglia (or basal nuclei) consist of multiple subcortical nuclei,
of varied origin, in the brains of vertebrates, which are situated at the base of
the forebrain. Basal ganglia nuclei are strongly interconnected with the cerebral
cortex, thalamus, and brainstem, as well as several other brain areas. The basal
ganglia are associated with a variety of functions including: control of voluntary motor
movements, procedural learning, routine behaviors or "habits" such as bruxism, eye
movements, cognition and emotion. The cerebellum (Latin for "little brain") is a major
feature of the hindbrain of all vertebrates. Although usually smaller than
the cerebrum, in some animals such as the mormyrid fishes it may be as large as or
even larger. In humans, the cerebellum plays an important role in motor control and it
may also be involved in some cognitive functions such as attention and language as
well as in regulating fear and pleasure responses, but its movement-related functions
are the most solidly established. The human cerebellum does not initiate movement,
but contributes to coordination, precision, and accurate timing: it receives input
from sensory systems of the spinal cord and from other brain parts & integrates these
inputs to fine-tune motor activity. Cerebellar damage produces disorders in fine
movement, equilibrium, posture & motor learning in humans.

97
Parkinson’s Disease.
should be able to:
 Understand what is meant by the term ‘Basal Ganglia’
 Outline neural structures that constitute the Basal Ganglia
 Understand the general connections between constituentnuclei
of the Basal Ganglia
 Understand how disruption in connections of Basal Ganglia nuclei
can give rise to Motor Deficits
 Understand the pathophysiology of Parkinson’s Disease
This session will be a lecture-demonstration similar in format to that on
lesions of the motor system, but here, we will consider presentational
signs consequent upon damage of the basal ganglia, giving rise to the
diagnosis of Parkinson’s Disease. The lecture-demonstration will be
preceded by an introduction to terms whereby florid symptoms/signs of
this disorder will be reviewed and the ways they are looked for, during
clinical assessment.
In the table below the florid features are described, whilst you watch the
video, tick in the table below, whether the various features are absent
(A) / just discernible (D) / clear (C) / florid (F), in the patients
illustrated.

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