Download The Nervous System

The Nervous System
Question
What is a group of axons travelling
together in the CNS called
What does the CNS consist of
What does a neurone cell body (soma)
contain
What are dendrites
What is the function of dendrites
What is the region called where the axon
connects to the cell body, what is its
function
Which part of a neurone is responsible
for releasing neurotransmitters
What type of neurones are unipolar
Where can you find bipolar neurones
What type of neurones are motor
neurones & interneurones
What are the myelin forming cells called
in the brain & spinal cord
What forms individual myelin sheaths in
the peripheral nervous system
What are nodes of ranvier
What is the function of a myelin sheath
What do glial cells surround
What is the function of glial cells
What are the different types of glial cells
What are the functions of astrocytes
What molecules can cross the BBB
What are the functions of microglia
What do microglia contain to help them
perform their function
Where do you find ependymal cells
What is the function of ependymal cells
Where are the meninges
What are the 3 membranes making up
the meninges
What is in the subarachnoid space
Answer
Pathway or tract – no nerves in CNS
Brain
Spinal cord
Nucleus & ribosomes – has genetic information & machinery for
protein synthesis
Multiple mitochondria, RER, free ribosomes, golgi apparatus,
lysosomes, vesicles
Highly branched outgrowths of the cell body
Receive most of the inputs from other neurones = site for synapses,
↑ s.area for receiving signals
Initial segment/axon hillock – triggers most of the electrical signals
Axon terminal
Sensory neurones
Retina
Multipolar
Oligodendrocytes
Schwann cells
Spaces between the myelin sheaths on peripheral nerves
Speeds up the conduction of electrical signals along the axon &
conserves energy
Soma, axon & dendrites of neurones
Physically & metabolically support neurones
Oligodendrocytes
Astrocytes
Microglia
Ependymal cells
Help regulate composition of ECF in the CNS by removing K+ &
neurotransmitters around synapses
Stimulate the formation of tight junctions between the cells that
make up the walls of capillaries – forming BBB
Involved in the transport of substances from blood to neurones
Sustain neurones metabolically by providing glucose
Guide neurones as they migrate to their ultimate destination in
developing embryos
Small molecules like O2, CO2, H2O
They are a specialised macrophage-like cell that perform immune
functions in the CNS, they coalesce in areas of damage
Lysosomes
They line fluid filled cavities within the brain & spinal cord
Produce & regulate the production & flow of CSF
Between the soft neural tissues of the brain & spinal cord & the
bones that house them
Thick dura mater next to the bone
Arachnoid mater in the middle
Thin pia mater next to the nervous tissue
CSF
1
What is the subarachnoid space between
What are the functions of the meninges
What cells is CSF produced by
Where are the cells that produce CSF
What system does the CSF circulate
through to the brainstem
Where does the CSF ultimately flow to,
why
Where do the dural sinuses drain to
What are the 2 layers of the dura mater
What is the embryological origin of the
CNS
Where is the tubule structure in the brain
Where is the tubular structure in the
spinal cord
What are the 4 ventricles in the brain
How are the lateral ventricles connected
to the 3rd ventricle
How is the 3rd ventricle connected with
the 4th ventricle
What forms the dorsal wall of the 4th
ventricle
What is the volume of CSF
What reabsorbs CSF
What are the factors favouring
reabsorption of CSF
What happens to the neural tube in the
4th week of development
What are the 3 prominent brain vesicles
from the neural tube, what do they
become
What does the Prosencephalon further
divide into, what do these divisions
become
What does the Rhombencephalon further
divide into
What is the shell of the cerebral cortex
made up of
What connects the left & right cerebral
hemispheres
What divides the diencephalon in 2
What does the diencephalon contain
What is the function of the thalamus
What is the function of the hypothalamus
What is the function of the brain stem
What does the brain stem consist of
The arachnoid & pia
Protect & support the CNS – circulate & absorb the CSF
Ependymal cells
They make up a specialised epithelial structure = choroid plexus
Interconnected ventricular system
The top of the outer surface of the brain, where most of it enters the
blood stream through one way valves in large veins
Internal jugular veins
Periosteal layer
Internal meningeal layer
Neural tube
Ventricular system
Narrow central canal
2 lateral ventricles
3rd ventricle
4th ventricle
Interventricular foramen
Cerebral aqueduct
Cerebellum
150ml
Arachnoid villi – located along the length of the dural venous sinus
Higher hydrostatic pressure in the CSF
Higher oncotic pressure in the blood
3 areas in the cephalic portion of the tube enlarge creating 3
prominent brain vesicles
Prosencephalon = forebrain
Mesencephalon = midbrain
Rhombenephalon = hind brain
Telencephalon = cerebrum
Diencephalon
Metancephalon = cerebellum & pons
Myelencephalon = medulla oblongata
Outer layer of grey matter
Inner layer of white matter
The corpus callosum
The 3rd ventricle
Thalamus
Hypothalamus
Collection of several large nuclei that serve as synaptic relay
stations & important integrating centres for most inputs to the cortex
Maintain homeostasis - Master command centre for neural &
endocrine coordination, it lies directly above the pituitary gland &
modulates its function, coordinates the limbic system
Relays information to or from cerebrum or cerebellum
Mesencephalon
Pons
Medulla oblongata
2
Why is the pons a ‘bridge’
What does the pons contain
What is the function of the cerebellum
Where does the spinal cord connect to
the brainstem
What are the functions of the medulla
oblongata
How does arterial blood reach the brain
How does most of the venous blood from
the brain leave the cranium
What are the internal carotid arteries
branches of
How do the internal carotid arteries enter
the skull
What are the vertebral arteries branches
of
How do the vertebral arteries enter the
cranium
Where is blood to brainstem &
cerebellum derived from
Where is blood to the cerebrum derived
from
What forms the circle of willis
What does the anterior cerebral artery
supply
What does the middle cerebral artery
supply
What does the posterior cerebral artery
supply
Which is the largest region of the brain
What originates in the cerebral
hemispheres (processes)
What happens to somatic sensory
information relayed to the brain
What are gyri
What are sulci
What are fissures
What is the purpose of gyri & sulci
Why does the cerebral cortex need lots
of neurones
What does each cerebral hemisphere
receive
What does each cerebral cortex generate
What is in the Frontal lobe of the cerebral
cortex
What is in the Parietal lobe of the
cerebral cortex
What is in the Occipital lobe of the
cerebral cortex
What is in the temporal lobe of the
cerebral cortex
Bridge between cerebellum & brain stem
Nuclei involved with both somatic & visceral motor control
Automatically adjusts motor activities on the basis of sensory
information & memories of learned patterns of movement = control
of balance, posture/muscle tone, coordination of movement
At the medulla oblongata
Relays sensory information to the thalamus & to other brainstem
centres
Contains major centres concerned with the regulation of autonomic
function e.g. heart rate, blood pressure, digestive activities
Through the internal carotid arteries & the vertebral arteries
In the internal jugular veins which drain into the dural sinuses
Common carotid artery
Through the carotid foramen
1st branch of subclavian arteries
Through forum magnum with the spinal cord
Branches of vertebro-basilar system
Circle of Willis – an anastamosing system of arteries
Internal carotid & basilar arteries
Medial aspect of cerebral hemispheres excluding occipital lobe
Lateral aspect of cerebral hemispheres
Inferior aspect of cerebral hemispheres & occipital lobe
The cerebrum
Conscious thought processes & all intellectual functions
It reaches out conscious awareness & cerebral neurones exert direct
or indirect control over somatic motor neurones
Elevated ridges on the cortical surface
Shallow compressions on the cortical surface
Deeper grooves on the cortical surface
Increase surface area of cerebral hemispheres – providing additional
space for adrenal cortical neurones
It performs complicated neural functions and analytical activities
requiring large numbers of neurones
Sensory information form the opposite side of the body
Motor commands to the opposite side of the body
Primary motor cortex – conscious control of skeletal muscles (&
personality)
Primary sensory cortex – conscious perception of touch, pressure,
vibration, pain, temperature & taste
Visual cortex – conscious perception of visual stimuli
Auditory & olfactory cortex – conscious perception of auditory &
olfactory stimuli
3
Where are the association areas in the
cerebral cortex
What happens in association areas
What happens in the precentral gyrus
What happens in the postcentral gyrus
What processes do you have dominant
hemispheres for
What do you have non-dominant
hemispheres for
What happens in Brocas’ area
Where is Brocas’ area
What happens in Wernickes’ area
Where is Wernickes’ area
What does the central white matter of the
cerebral cortex contain
What are association fibres for in the
central white matter
What are commissural fibres for in the
central white matter
What are projection fibres
Where are the basal nuclei
What are the basal nuclei
What processes are basal nuclei
involved in
Do the basal nuclei initiate movements
What do the basal nuclei do in the control
of movements
For which movements of the body are
the basal nuclei particularly important
What is the function of the striatum
What is the function of the Globus
Pallidus
Name the basal ganglia/nucleus
What is the grey area of the spinal cord
composed of
What does the white matter of the spinal
cord contain
On which side of the cord do afferent
fibres enter
Where are the cell bodies of afferent
neurones
Where do the efferent neurones leave
the spinal cord
What forms each spinal nerve
What does the peripheral nervous
system transmit information between
How many pair of nerves are in the PNS
In all of the lobes
Integration & processing of sensory data, processing & integration of
motor activities
Initiation of voluntary motor functions
It is involved in somatic sensation
Language skills
Mathematical reasoning
Spatial awareness
Musical skills
Production of words (including written)
Inferior frontal gyrus, dominant hemisphere
Understanding of words
Posterior, superior temporal gyrus
Myelinated fibres that form bundles that extend from one cortical
area to another, or that connect areas of the cortex to other areas of
the brain
Interconnect portions of the cerebral cortex within the same cerebral
hemisphere
They connect the 2 cerebral hemispheres
They are tracts which link the cerebrum with other regions of the
brain & spinal cord
Within the cerebral hemispheres, embedded within the central white
matter
Paired masses of grey mater
The subconscious control of skeletal muscle tone & the coordination
of learned movement patterns
No
Provide general pattern & rhythm once the movement is underway
Trunk and proximal limb movements
Caudate nucleus & putamen– controls cycles of arm & leg
movements that occur between the decision to start & stop walking
Controls & adjusts muscle tone, particularly in appendicular muscles
to set body position for voluntary movement
Caudate nucleus
Putamen
Globus pallidus
Subthalamic nucleus
Substantia nigra
Interneurones, the cell bodies & dendrites of efferent neurones, the
entering axons of afferent neurones & glial cells
Groups of myelinated axons
Dorsal side via the dorsal roots
Dorsal root ganglia
On the ventral side via the ventral roots
The dorsal & ventral roots combining
The CNS & receptors & effectors
43
4
How many of these nerves are spinal
What are the remaining nerves
How many pairs of cervical nerves
What do cervical nerves do
How many pairs of thoracic nerves are
there
What are the thoracic nerves associated
with
How many pairs of lumbar nerves are
there
What are the lumbar nerves associated
with
How many pairs of sacral nerves are
there
What are the sacral nerves associated
with
What do all spinal nerves contain
How do cranial nerves differ from spinal
nerves in what they contain
Why can afferent neurones be called
primary afferents or first order neurones
Why is the efferent NS more complicated
than the afferent NS
What do somatic nerves do
What do autonomic nerves do
How do the chains in a pathway run
together
Where do sensory pathways carry
information to (1 exception)
What order of neurones are
interneurones
What are ‘specific ascending pathways’
What happens to specific pathways from
the right side of the body
Where do you find somatic receptors
Where do specific ascending pathways
that transmit information from somatic
receptors go
Where do the specific pathways from the
eyes go
Where do the specific pathways from the
ears go
What happens to afferent information
after they have been through the primary
cortical receiving areas
How do neurones in non-specific
ascending pathways differ from those in
ascending pathways
What are polymodal (inter)neurones
31
12 cranial
8
Control the muscles & glands & receive sensory information input
from the neck, shoulder, arm & hand
12
Chest & abdominal wall
5
Hips & legs
5
Genitals & lower digestive tract
Afferent & efferent fibres
Some cranial nerves contain only afferent fibres
They are the first cells entering the CNS
The efferent NS is subdivided into somatic & autonomic
Innervate skeletal muscle
Innervate smooth muscle, cardiac muscle, glands & neurones in GI
tract
In parallel
Cerebral cortex – responsible for conscious recognition
Second order
Ascending pathways in the spinal cord and brain that carry
information about single types of stimuli – these pass to the
brainstem & thalamus – then to specific sensory areas of the
cerebral cortex
They cross over to the opposite side of the nervous system –
information from receptors on the right side of the body is
transmitted to the left cerebral hemisphere
Skin, muscles, tendons & joints
To the somatosensory cortex
The visual cortex in the occipital lobe
Auditory cortex in the temporal lobe
Continue to association areas in the cerebral cortex where complex
integration occurs
Neurones in non-specific ascending pathways are activated by
sensory units of different types and signal general information (don’t
specify what or where)
(Inter)neurones that respond to input from several afferent neurones
each activated by a different stimulus
5
Where do non-specific ascending
pathways end
How many neurones are involved in
sensory pathways ending in the cerebral
cortex
How many neurones are involved in
sensory pathways ending in the
cerebellum
What are 2 properties of pathways
involving the major sensory & motor
tracts of the spinal cord
What are first order neurones
What are second order neurones
What are third order neurones
The axon of which neurones is involved
in decussation
What is a dermatome
What is a myotome
Which part of a spinal nerve provides
sensory innervation
Why is cutaneous nerve distribution
different from dermatomes
What is carried in the spinothalamic tract
Where do 1st order neurones in the
spinothalamic tract synapse
Where do 2nd order neurones decussate
What happens to the 2nd order neurones
in the brainstem
Where do sympathetic nerves leave the
CNS
Where do parasympathetic nerves leave
the CNS
What happens above a lesion in a
peripheral nerve (lower motor neurone
injury)
What happens below a lesion in a lower
motor neurone injury
What happens above a lesion in an
upper motor neurone injury
What happens at the level of a lesion in
an upper motor neurone
What happens to muscle tone and
reflexes below a lesion in an upper motor
neurone
What happens to power, sensation and
coordination below a lesion in an upper
motor neurone
Which type of fibres decussate almost
immediately on entering the spinal cord
In parts of the brainstem & regions of the thalamus & cerebral cortex
that are not highly discriminative but are important in controlling
awareness & arousal
3
2
The tracts are paired
Axons within each tract are grouped according to the body region
innervated
Sensory neurones that deliver the sensations to the CNS
CNS neurones on which 1st order neurones synapse
2nd order neurones synapse onto them in the thalamus
Either first or second order neurones
A specific region of the body monitored by a pair of spinal nerves =
area of skin where sensation is supplied by one spinal nerve
Relates to the muscles which share the motor supply of one spinal
segment (most muscles belong to more than one myotome)
Dorsal ramus
Each cutaneous nerve may receive nerve fibres derived from a
number of different dermatomes, and/or the nerve fibres from one
dermatome may be dispersed amongst a number of cutaneous
nerves
Fibres related to pain, temperatre, non-discriminatory touch &
pressure
Within the dorsal horn
Prior to ascending in the spinothalamic tract
Run in the spinal lemniscus to the thalamus
T1 – L2
Cranial 3,7,9 & 10
Sacral 2-4
Above lesion everything is normal
Below a lesion everything is absent or decreased
Above lesion everything is normal
Everything absent or decreased
It is increased – because inhibitory neurones from premotor nerves
are cut off
Absent or decreased
Pain and temperature fibres
6
Cranial nerves
What are cranial nerves
How many pairs of cranial nerves are
there
Which surface of the brain can they be
found on
How are cranial nerves numbered
What is CNI
What is the primary function of CNI
What is the origin of CNI
What is the destination of CNI
What is special about CNI
What is CNII
What is the primary function of CNII
What is the origin of CNII
What is the destination of CNII
What is CNIII
What is the primary function of CNIII
What is the origin of CNIII
What is the destination of CNIII
What is CNIV
What is the primary function of CNIV
What is the origin of CNIV
What is the destination of CNIV
What is special about CNIV
What is CNV
What is the primary function of CNV
What are the branches of CNV and what
are their functions
What is the origin of CNV1
What is the origin of CNV2
What is the origin of CNV3
What is the destination of CNV
What is special about CNV
What is CNVI
What is the primary function of CNVI
What is the origin of CNVI
What is the destination of CNVI
What in CNVII
What is the primary function of CNVII
What is the origin of CNVII
What is the destination of CNVII
Components of the PNS that connect to the brain rather than the
spinal cord
12
Ventrolateral surface
According to their position along the longitudinal axis of the brain,
beginning at the cerebrum
The Olfactory nerve
Special sensory = smell
Receptors of the olfactory epithelium
Olfactory bulbs
Only cranial nerve attached directly to the cerebrum
The Optic nerve
Special sensory
Retina of the eye
Diencephalons by way of the optic chiasma
The Oculomotor nerve
Motor, eye movements
Mesencephalon
Somatic motor: superior, inferior & middle rectus muscles, levator
palpebrae superioris
Visceral motor: intrinsic eye muscles
The Trochlear nerve
Motor, eye movements
Mesencephalon
Superior oblique muscle
It is the smallest of all the cranial nerves
The Trigeminal nerve
Mixed – sensory & motor
CNV1 Ophthalmic branch = sensory
CNV2 Maxillary branch = sensory
CNV3 Mandibular branch = sensory & motor
Orbital structures, nasal cavity, skin of forehead, superior eyelid,
eyebrow, part of nose
Inferior eyelid, upperlid, gums, teeth, cheek, nose, palate, part of
pharynx,
Sensory: lower gums, teeth, lips, palate, tongue (part)
Motor: motor nuclei of pons
All branches to sensory nuclei in the pons
Mandibular branch also innervates muscles of mastication
It is the largest cranial nerve
The Abducens nerve
Motor, eye movements
Pons
Lateral rectus muscle (6th intrinsic eye muscle)
The Facial nerve
Mixed – sensory & motor
Sensory: taste receptors on anterior 2/3rd of tongue
Motor: motor nuclei of pons
Sensory: sensory nuclei of pons
Somatic motor: muscles of facial expression
Visceral motor: lacrimal (tear) gland, nasal mucous glands,
submandibular & sublingual salivary glands
7
What is Bells palsy
What are the symptoms of Bells palsy
What is CNVIII
What is the primary function of CNVIII
What are the branches of CNVIII and
what are their functions
What is the origin of CNVIII
What is the destination of CNVIII
What in CNIX
What is the primary function of CNIX
What is the origin of CNIX
What is the destination of CNIX
What is CNX
What is the primary function of CNX
What is the origin of CNX
What is the destination of CNX
What is CNXI
What is the primary function of CNXI
What is the origin of CNXI
What is the destination of CNXI
What is CNXII
What is the primary function of CNXII
What is the origin of CNXII
What is the destination of CNXII
How does CNI enter the cranium
How does CNII enter the cranium
How does CNIII exit the cranium
How does CNIV exit the cranium
How does CNV1 exit the cranium
How does CNV2 exit the cranium
How does CNV3 exit the cranium
How does CNVI exit the cranium
How does CNVII exit the cranium
How does CNVIII exit the cranium
How does CNIX exit the cranium
How does CNX exit the cranium
How does CNXI exit the cranium
How does CNXII exit the cranium
Which part of the brain does CNIII
emerge from
Which part of the brain does CNIV
emerge from
Which part of the brain does CNV1
emerge from
An inflammation of the facial nerve
Paralysis of facial muscles on the affected side & loss of taste
sensations from anterior 2/3 of the tongue
The Vestibulocochlear nerve
Special sensory
Vestibular branch: balance & equilibrium
Cochlear branch: hearing
Receptors of the inner ear
Vestibular & cochlear nuclei of pons & medulla oblongata
The Glossopharyngeal nerve
Mixed – sensory & motor
Sensory: posterior 1/3 of the tongue, part of the pharynx, palate,
carotid arteries (carotid body & carotid sinus)
Motor: motor nuclei of medulla oblongata
Sensory: sensory nuclei of medulla oblongata
Somatic motor: pharyngeal muscles involved in swallowing
Visceral motor: parotid salivary gland
The Vagus nerve
Mixed: sensory & motor
Visceral sensory: pharynx, auricle, external acoustic meatus,
diaphragm & visceral organs in thoracic & abdominopelvic cavities
Visceral/somatic motor: motor nuclei in medulla oblongata
Visceral Sensory: sensory nuclei & autonomic centres of medulla
oblongata
Somatic motor: muscles of palate & pharynx
Visceral motor: respiratory, cardiovascular & digestive organs
The Accessory nerve
Motor (soft palate, throat & neck)
Motor nuclei of spinal cord & medulla oblongata
Internal branch (branchial motor): voluntary muscles of palate,
pharynx & larynx
External branch (somatic motor): sternocleidomastoid & trapezius
The Hypoglossal nerve
Motor, tongue movements
Motor nuclei of the medulla oblongata
Muscles of the tongue
Through foraminifera in cribriform plate of ethmoid bone
Enters via optic canal, nerves join to form optic chiasma
Via superior orbital fissure
Via superior orbital fissure
Via superior orbital fissure
Via the foramen rotundum
Via the foramen ovale
Via superior orbital fissure
Internal acoustic meatus, facial canal & stylomastoid foramen
Internal acoustic meatus
Via the jugular foramen
Via the jugular foramen
Via the jugular formanen
Through the hypoglossal canal
Midbrain
Dorsal surface of midbrain
Pons
8
Which part of the brain does CNV2
emerge from
Which part of the brain does CNV3
emerge from
Which part of the brain does CNVI
emerge from
Which part of the brain does CNVII
emerge from
Which part of the brain does CNVIII
emerge from
Which part of the brain does CNIX
emerge from
Which part of the brain does CNX
emerge from
Which part of the brain does CNXI
emerge from
Which part of the brain does CNXII
emerge from
Which cranial nerve is concerned with
smell
Which cranial nerve is concerned with
sight
Which cranial nerves are concerned with
taste
Which cranial nerve is concerned with
hearing & balance
Which cranial nerve is concerned with
movement of the eyes
Which cranial nerve is concerned with
movement of face
Which cranial nerve is concerned with
sensation from the face
Which cranial nerve is concerned with
chewing
Which cranial nerve is concerned with
swallowing
Which cranial nerve is concerned with
movement of the tongue
Which cranial nerve is concerned with
movement of the vocal cords
Which cranial nerve is concerned with
parasympathetic visceral sensory input
Which cranial nerve is concerned with
movement of the neck
Where are cell bodies of efferent
neurones
Where are cell bodies of afferent
neurones
What is a collection of cell bodies in the
periphery called
What is a collection of cell bodies in the
CNS called
What is the Io function of the olfactory
nerve
What is the Io function of the optic nerve
Pons
Pons
Between pons & medulla
Between pons & medulla
Between pons & medulla
Medulla
Medulla
Small cranial roots (medulla) and large spinal roots
Medulla
Olfactory
Optic
Facial
Glossopharyngeal
Vagus
Vestibulocochlear
Oculomotor
Trochlear
Abducent
Facial
Trigeminal
Trigeminal (mandibular)
Glossopharyngeal
Accessory
Hypoglossal
Vagus
Vagus
Accessory
Outside CNS
Inside CNS
Ganglion
Nucleus
Sensory (smell)
Sensory (sight)
9
What is the Io function of the oculomotor
nerve
What is the Io function of the trochlear
nerve
What is the Io function of the trigeminal
nerve
What is the Io function of the abducent
nerve
What is the Io function of the facial nerve
What is the Io function of the
vestibulocochlear nerve
What is the Io function of the
glossopharyngeal nerve
What is the Io function of the vagus nerve
What is the Io function of the accessory
nerve
What is the Io function of the hypoglossal
nerve
Motor System
What are lower motor neurones
What happens if you get lesions in lower
motor neurones
What are upper motor neurones
What do upper motor neurone lesions
cause
What happen in corticospinal lesions
What is the direct control of muscles
Where do segmental reflexes occur
What further control are segmental
reflexes subject to
Which descending inputs are important in
the control of muscle groups of the trunk
& limbs
What are the brainstem nuclei controlled
by
what is the direct cortical connection to
the spinal cord
What are the higher brain centres
involved in motor control
What is the sensory input to the
brainstem from
What happens if sensory inputs are
damaged at a spinal level
How can the segmental reflex be
influenced by higher centres
How can input to the α motorneurones
effect the stretch reflex
How can input to the γ motor neurones
effect the stretch reflex
How can input to the interneurones effect
the stretch reflex
What is α-γ coactivation
Motor (eye movements)
Motor (eye movements)
Mixed (sensation from face & mouth, motor for muscles of
mastication)
Motor (eye movement)
Mixed (muscles of facial expression, parasymp, taste)
Sensory (hearing & balance)
Mixed (swallowing, sensation from tongue, parasym)
Mixed (muscles of throat, parasym, visceral sensory)
Motor (soft palate, throat & neck)
Motor (movement of the tongue)
Spinal & cranial nerves that directly innervate muscles
Flaccid paralysis & atrophy
Neurones in the brain & spinal cord that change α motorneurone
activity
Spasticity, some paralysis
Weakness (paresis), rather than paralysis
Via α motorneurones in the ventral horn of the spinal cord
At the spinal cord level
Further control via brainstem nuclei, which organise them into higher
order reflexes, involved in the control of posture & balance
Vestibulospinal and the reticulospinal tracts
Higher brain centres
Corticospinal tract (AKA pyramidal tract)
Cerebral cortex (motor cortex & association areas, premotor &
supplementary motor areas)
Basal ganglia
Cerebellum
Vestibular system
Paralysis as if the motor neurones themselves had been damaged
Directly onto α motor neurones
By acting on γ motorneurones
By acting on interneurones
if they are strongly inhibited by descending voluntary input the
stretch reflex can be overridden
Descending input onto γ motorneurones can change the sensitivity
of the spindles
They can influence the balance between agonist & antagonist
The α motorneurones are activated to make the desired movement
and γ motorneurones are activated at the same time to maintain the
10
What is the crucial cord segment in the
biceps jerk
What is the crucial cord segment in the
triceps jerk
What is the crucial cord segment in the
patellar tendon
What is the crucial cord segment in the
Achilles tendon reflex
What is the significance of testing
reflexes
What is the Babinski sign
What can cause flexor reflexes in certain
sensitive parts of the body
Which normal healthy group show the
Babinski sign
When can the Babinksi sign be seen in
epileptics, why
What is most of the human cerebral
cortex
What is the main motor area in the
cerebral cortex
What is the main motor area right next to
What do cortical cells give rise to
What are the cell bodies of cortical
neurones like
What % of the CS tract neurones are
myelinated
Where is the major decussation of the
CS tract
What % of the axons cross over
What is the motor homunculus
What sort of movements is the motor
cortex involved in
What does damage to the motor cortex/
CS cause
Is the motor cortex involved in the
initiation of movement
What is the readiness potential
What happens about 50ms before the
movement actually occurs
Why are patients surprised if you
stimulate the motor cortex
What is the function of the premotor
cortex
What is the function of the
supplementary motor area
Where can ↑ in electrical activity & blood
flow be seen when rehearsing complex
motor tasks
What are the supplementary motor area
and the premotor cortex part of
sensitivity of the spindles to length changes
C6
C7
L4
S1
Helps detect level of spinal cord damage – ability to evoke reflexes
above but not below a certain level
Impaired reflexes may indicate nerve damage
Shows damage or disruption to CS tract, stroking along lateral
aspect of foot causes toes to fan up and out
Mild cutaneous stimulation
Children < 1 year old whose motor system is not fully developed
Transiently following an epileptic fit when cortical function is still
disrupted
Association cortex involved in complex processing
Precentral gyrus
Somatosensory area
CS projections to α and γ motorneurones
Large, pyrimdal shaped
50%
In the brainstem
80%
A topographic orderly mapping of the motor representation of the
body on the motor cortex
Fine precision voluntary movements
Clumsiness
No
An ↑ in electrical activity in all cortical and some subcortical ones
before a voluntary movement starts (thinking about it)
Extra burst of activity in motor cortex which controls muscles needed
for the desired movement = signals being sent down CS tract to
activate motorneurones
They move but without the thinking about it stage
It is responsible for identifying goals and choosing a course of action
Involved in the programming of voluntary movements
Supplementary motor area
The association cortex
11
What is the function of the posterior
parietal cortex (PPC)
What happens if there is a lesion in the
PPC
What are the 2 main parts of the Basal
Ganglia
What is the Striatum divided into
What does the Striatum receive, what
does it do with this
Which 2 midbrain nuclei do the basal
ganglia connect to
What are Basal ganglia involved in
What so diseases of the Basal ganglia
manifest as
What type of disorder in Parkinson’s
disease
What are the features of Parkinson’s
disease
What is superimposed on the main
disorder in Parkinson’s disease
What are the symptoms of this imposed
disorder
What type of disorders are Huntington’s
Chorea, Athetosis and Ballism
What are the symptoms of Huntington’s
Chorea
What are the symptoms of Athetosis
What are the symptoms of Ballism
Describe the main feature of cells of the
Pallidum
In mind of the above, what is control of
movement
What is the controlling feature of the
striatum
What neurotransmitter does the striatum
use
Where does organising cortical input
arrive via
What are the processes going on to keep
a person at rest
What happens when a voluntary
movement is to be initiated
What happens to cause Huntington’s
Chorea
What happens to cause Ballism
What keeps the inhibitory pathway from
the striatum to the pallidum in check
Essential for the processing of sensory stimuli leading to purposeful
movements
“neglect syndrome” – an inability to respond to stimuli on the
contralateral side of the body – patients may deny contralateral limb
is theirs
Striatum
Globus pallidus (pallidum)
Caudate
Putamen
A copy of the readiness potential, which is processed by the striatum
& pallidum then relayed via the thalamus to the cortex & premotor
cortex
Substantia nigra
Subthalamic nucleus
Processing the readiness potential so that initiation of voluntary
movement can occur
Difficulties in starting voluntary movements and stopping unwanted
movements
Hypokinetic disorder – there is akinesia
Extreme difficulty in starting voluntary movements, also a lot of
associated movements e.g. swinging arms when walking, loss of
facial expression
Hyperkinetic features
Resting tremor = shake at rest, tremor disappears when movement
is in progress
Rigidity - ↑ muscle tone which affects both flexors & extensors
Hyperkinetic disorder
Jerky spasmodic movements at ‘rest’ and incorporated into ‘normal’
voluntary movements
Slow writhing movements which affect the extremities – adopt
grotesque postures
Violent flailing of the limbs
They have a high level of spontaneous activity
Voluntary regulation of this spontaneous activity
It exerts a profound inhibitory effect on the pallidum
GABA
The striatum
The ‘organising cortical input’ excites the striatum, which then
inhibits the pallidum
Patterned inhibition in the form of the readiness potential allows
organised excitation to be transferred from the pallidum to the motor
cortex
There is striatal degeneration, so that the organising cortical input is
lost, so the spontaneous activity of the pallidum passes unchecked
to the MC
There is degeneration of the subthalamic nucleus, releasing pallidal
activity
The inhibitory pathway from the substantia nigra to the striatum =
nigrostriatal pathway
12
What is the function of keeping the above
pathway in check
What neurotransmitter does the above
pathway use
What happens to cause Parkinson’s
disease
What is the main characteristic of
Parkinson’s disease
What % of SN neurones degenerate
before clinical symptoms of Parkinson’s
appear
In treating Parkinson’s disease what are
you trying to compensate for
Why do you give L-DOPA
What is the problem with giving L-DOPA
How can the efficacy of L-DOPA be
improved
What catalyses the breakdown of LDOPA
How long is L-DOPA affective in treating
Parkinson’s
What can long term treatments with LDOPA or other DA agonists produce
What is schizophrenia associated with
What are the ‘possible’ new treatments
for Parkinson’s
What is the pathway that produces DA,
what can DA go on to produce
What are the 2 parts to the inhibitory
striatal pathway to the pallidum
Why can drugs which block ACh be
effective at ↑ the effective of remaining
dopaminergic neurones
What is the aim of the treatment of
Huntington’s chorea
What sort of treatments are used in
Huntington’s chorea
What can be the side effects of the drugs
used to treat Huntington’s chorea
How is Huntington’s disease inherited
Cerebellum
What is the cerebellum responsible for
What is co-ordination
What is the structure of the cerebellum
What are the 3 functional parts of the
cerebellum
What is the function of the
archicerebellum
It ensures that the pallidum does not get too much inhibition
Dopamine
Degeneration of the substantia nigra pathway
It is very hard to initiate a voluntary movement
>80%
Loss of domaminergic neurones
L-DOPA is the precursor of dopamine, L-DOPA can cross the BBB
but dopamine can’t
It is taken up by many tissues in the body so that < 0.01% of an oral
dose reaches the substantia nigra
Combining L-DOPA with a selective extra-cerebral decarboxylase
inhibitor, which reduces peripheral breakdown
L-DOPA → dopamine, catalysed by DOPA decarboxylase
5-7 years
Symptoms of psychosis
Overactivity of dopaminergic pathways
Autotransplantation of adrenal medulla (DA is precursor of NE)
Foetal transplants
Target viruses to carry tyrosine hydroxylase gene to sites of DA
synthesis
Stem cells
Phenylalanine → Tyrosine → L-DOPA → Dopamine → N.E → E
Striatal cholinergic interneurones onto inhibitory GABA neurones
from the striatum to the pallidum
Both the cortical input & nigrostriatal inhibition are onto striatal
cholinergic neurones
↑ efficacy of remaining striatal interneurones
ACh mimetics & DA blockers
They may produce Parkinsons
As an autosomal dominant disease
Co-ordination of voluntary movements
Control of the timing of sequences of contractions in different
muscles to make a movement smooth & reliable
Highly convoluted grey matter cerebellar cortex, beneath which is
white matter containing axons going to & from the cortex. Embedded
in the white matter are the deep cerebellar nuclei
Archicerebellum (vestibulocerebellum)
Paleocrebellum
Neocerebellum
Oldest part – concerned with posture & balance, major input from
vestibular system
13
What is the function of the
Paleocerebellum
What is the function of the
neocerebellum
What is the largest functional part of the
cerebellum in man
Where is all input to the cerebellum to
Where is all cerebellar output from
What are the 2 routes via which
information can reach the cortex
What are the connections from the pons
to the cerebellar cortex
What are the connections from the
inferior olive to the cerebellar cortex
What does the cerebellum receive from
the CS tract, via what
What is the major input to the cerebellum
What causes an error signal
Where is an error signal sent to
What does the cerebellum carry, which is
the same simple circuitry repeated
millions of times
What cells are the only output of the
cerebellar cortex
What do mossy fibres connect with
What happens when mossy fibres make
their connections
What do indirect climbing fibres make
connections with
What happens when indirect fibres make
their connections
What is motor learning about
What causes synaptic strengthening
What is the result of synaptic
strengthening
Are climbing fibres needed when the
movement becomes automatic
Is synaptic strengthening permanent
How is co-ordination achieved
What is the result of purkinje cell
discharge
What is passed from the dentate nucleus
to the MC
What is ataxia
How does cerebellar damage affect the
appearance movements
How can cerebellar damage affect
muscles
What tremor is associated with cerebellar
damage
What is dysdiadochokinesia
Important in 4 legged animals for the control of gait
Unconscious co-ordination of voluntary movements
Neocerebellum – 90% in man
To the cortex, cerebellar hemispheres
The nucleus (dentate in the case of the neocerebellum), relayed via
the thalamus to the motor cortex
Direct route via pons of brainstem
Indirect route, which traverses several brain areas and finally makes
connections in the inferior olive of the brainstem
Mossy fibres
Climbing fibres
Collaterals of CS tract pass to cerebellum, copy of signals being
sent to the motor neurones
Readiness potential – copy of movement desired
A discrepancy between the readiness potential and the copy of the
signals being sent to the motor neurones
The motor cortex
Motor homunculus
Purkinje cells
Each mossy fibre makes connections with > 1000 purkinje cells
Mossy fibres raise the level of excitation in purkinje cells, but does
not cause APs to be generated (in the purkinje cells)
1:1 contact with purkinje cells
Cause APs in Purkinje cells which inhibit the dentate nucleus
Selecting the right climbing fibre to give you the effect that you want
It is a result of joint activation of mossy fibre & climbing fibre inputs
to a purkinje cell
Eventually mossy fibre input on its own is enough to cause APs to
be discharged in purkinje cells
No
Yes – it involves ↑ permeability to Ca2+ and protein synthesis
Mossy fibre excitation sweeps along the array of purkinje cells, there
is separation between their excitation, the purkinje cells picked out
by synaptic strengthening will discharge in a temporal pattern
It inhibits the discharge of the dentate nucleus (which also caused
by mossy fibre excitation)
A temporal code of excitation, caused by purkinje cells inhibiting the
discharge of the dentate nucleus
In-coordination
Ataxia
Decomposition of movement – e.g. joint by joint, also affects speech
Asynergia – lack of cooperation between agonists & antagonists,
they may contract together
Intentional tremor – occurs during a movement and particularly
towards the end – no tremor at rest
Inability to make rapid alternating opposite movements
14
Why does cerebellar damage affect
posture, gait and balance
Vestibular System
Where is the vestibular system found
What are labyrinths
What do labyrinths detect
What are the sensory cells in the
vestibular system
What features do these sensory cells
have
What causes these sensory cells to
discharge action potentials
What causes a decreased discharge of
AP from the sensory cells
What is tilt of the head detected by
What is side to side tilt detected by
What is forward to back tilt detected by
What are the cilia in macula organs
embedded in
How are otoliths different to endolymph
What happens to otoliths when the head
is tilted, what does this cause
What are the semi-circular canals
(SCCs) like
What are the swelling in the SSCs, what
is in them
What do sensory cells SSCs detect
What happens to the endolymph in SSCs
when the skull initially at rest is turned
How does the above affect the cilia
What happens if you rotate at a constant
velocity
What does the posterior SSC detect
What doe the anterior SSC detect
What does the horizontal SSC detect
What does information from the SSC &
macula organs pass along
Where does information from the SSC &
macula organs initially go to
What do vestubular nuclei project to in
the opposite cortex
What do vestibular nuclei also receive
input from
How do the vestibular nuclei contribute to
kinasthesia
What is kinaesthesia
What tracts are involved in reflexes
mediated by the vestibular system
What is the function of the ‘Tonic
labyrinthine reflex’
Where does the ‘Tonic labyrinthine reflex’
get its information from
Relates to use of information from the vestibular system – adopt
wide swaying gait
In the inner ear, it is a series of fluid-filled membranous tubes, which
are embedded in the temporal bone
A series of fluid-filled membranous tubes
Tilt of the head with respect to the body
Angular accelerations
Hair cells, whose cell bodies are embedded in the bone of the skull
They have a set of cilia, which protrude into the endolymph, there is
a large kinocilium and progressively smaller stereocilia
Distortion of the cilia in the direction of the kinocilium causes
depolarisation & ↑ discharge of AP
Distortion of the cilia away from the kinocilium leads to
hyperpolarisation & ↓ discharge of AP
Macula organs (utriculus & sacculus)
Utriculus
Sacculus
A blob of jelly which contains crystals of CaCO 3 = otoliths
Otoliths have a greater density than endolymph and so are not
effeted by gravity
The blob of jelly (otolith) is distorted causing shearing forces on the
cilia
They are like closed tubes of endolymph
Swellings = ampullae in which are the cupula organs (hair cells)
Angular acceleration
The endolymph at first tends not to move because of its inertia
The base of the cilia move because they are embedded in the bone,
this produces shearing forces which bend the cilia
The endolymph rotates at the same speed so there are no shearing
forces
Head over heals rotation
Side to side rotation
Spinning
CNVIII (vestibulochoclear) vestibular nerves
Vestibular nuclei & then make lots of connections
The other set of vestibular nuclei
Proprioceptors signalling limb & body position, also from neck & eye
muscles
Vestibular nuclei project via the thalamus to the cerebral cortex
Perception of movement & body position
Vestibulospinal tracts
Reticulospinal tracts
Keeps the axis of the head in a constant relationship with the rest of
the body
Macula organs and neck proprioceptors
15
What is the ‘Dynamic righting reflex’
What do the Vestibulocochlear reflexes
involve
What are the 2 vestibulocochlear reflexes
What is the ‘Static reflex’
What is the input to the ‘Static reflex’
What is the ‘Dynamic reflex’ another
name for
What is the ‘Dynamic reflex’
Why is the reflex dynamic
What causes a right nystagmus
What is the conventional direction of
nystagmus
What can nystagmus be used to test
What are the 22 tests that can be done
What is tested by caloric stimulation
What does washing with 44oC H2O cause
What does washing with 30oC H2O cause
What would be seen if you put warm
water into right ear
What ahs to be done to visual input to
test vestibular function
What can result from powerful
maintained stimulation of the vestibular
system
When is motion sickness most likely to
occur
What happens in motion sickness
How do trained ballerinas avoid motion
sickness
What are the symptoms of acute
interference of normal vestibular function
What is vertigo
What happens in Meniere’s disease
What’s Menieres disease associated with
Can vestibular impairement be
compensated for
What can cause nystagmus at rest
What is the dominant input to the
archicerebellum
EEG/Sleep
What are the 2 ways of assessing
someone’s consciousness
Rapid postural adjustments that are made to stop you falling when
you trip. Long reflexes, involving extension of all limbs
Eye movements & the control of the extraocular muscles
Static reflex
Dynamic reflex
When you tilt your head your eyes roll to compensate, so that over a
certain range, the image stays the right way up
Macula input plus proprioceptors from eye muscles
Vestibular nystagmus
A series of eye movements that rotate the eye against the direction
of rotation of the head so that the original direction of gaze is
preserved
The extent of eye movement is restricted, when eye muscles come
to the end of their range, they rapidly flick back to the zero position
straight ahead & the slow phase starts again
Right rotation
Same as the direction of rapid flick back
Vestibular function
Post-rotatory nystagmus (opposite direction to nystagmus during
rotation)
Caloric stimulation – outer ear washed with cold or warm fluid, temp
difference (from core temp) sets up convection currents which affect
endolymph
Horizontal SSC and associated circuitry
Nystagmus towards affected side
Nystagmus away from affected side
Right nystagmus
Get rid of visual input – patients wear Freznel’s spectacles which
prevent visual fixation
Kinetosis (motion sickness), nausea & vomiting, ↓ BP & dizziness,
sweating & pallor = all are autonomic NS symptoms
If visual & vestibular system inputs to the archicerebellum are in
conflict e.g. vestibular system indicates rotation but visual system
doesn’t
The archicerebellum generates a ‘sickness signal’ to the
hypothalamus to bring about the ANS changes
They learn to visually fixate
All ANS symptoms plus vertigo, there will also be nystagmus
The perception of movement in the absence of movement
Vertigo, nausea, nystagmus & tinnitus (subjective noise)
Over production of endolymph
Yes – by visual system
Lesions of the brainstem
Visual input
By their behaviour
By their brain activity
16
What can brain activity be analysed in
terms of
What is the EEG of the awake state
characterised by
What does amplitude show
What does frequency show
What is the α rhythm
What is the β rhythm
When do EEG have a low amplitude &
high frequency, why
What are the other names for REM sleep
What are other names for non-REM
sleep
What happens during S-wave sleep
How many stages of S-sleep are there
Which is the deepest stage of S-sleep
What NS is dominant in deep S-sleep
What happens at each successive stage
of S-sleep
How does sleep begin (stages)
What happens when deep S-sleep is
reached
What is the EEG of REM sleep like
Why is REM sleep called paradoxical
sleep
When is brain O2 consumption highest
What are the physiological signs during
REM sleep
When is dreaming likely to occur
What is the first period of REM sleep like
What happens to periods of REM sleep
throughout the night
What happens to S-sleep throughout the
night
What is stage 3 & 4 sleep
When does stage 3 & 4 sleep occur
What happens to total sleep time during
childhood & adolescence
What happens to REM sleep during life
What is chronic insomnia
What is the action of many hypnotic
drugs, especially barbiturates
What happens when the above drugs are
withdrawn
What are nightmares
What can be recorded during dreams
What do dreams do to the motor system
What are night terrors
Amplitude
frequency
Low amplitude, high frequency waves
The bigger the wave the more the activity of the cells is
synchronised
The higher the frequency, the faster the rate of fluctuations in the
cortical cells
In relaxed state with eyes closed – frequency becomes slower &
amplitude becomes greater
In the alert state – higher frequency & smaller amplitude
When cells are busy all doing different things rapidly, because they
are not synchronised
D-sleep, paradoxical sleep
Slow wave sleep, S-sleep
There is a gradual ↑ in amplitude of EEG waves as the activity of
more and more of the cells are synchronised and the frequency is
slow
4
4 – person is difficult to rouse
Parasympathetic dominance – e.g. ↓HR
As you move from 1→4 the EEG pattern develops a slower
frequency and higher amplitude
Progression from 1→4, normally takes 30-45 mins
The process reverses itself – there is a gradual awakening towards
stage 1 sleep but instead of stage 1 there is REM sleep
EEG waves are desynchronised, high frequency, low amplitude
It has an EEG very like the awake state but the sleeper is difficult to
rouse
During REM sleep
Profound inhibition of body muscles
Except for eye muscles which show bursts of activity
Sympathetic dominance - ↑ HR & BP, ↑ cerebral BF, ↑ brain
temperature
During REM sleep
Short – 5 – 10 mins
REM periods increase in duration throughout the night
It becomes shallower
Delta sleep – restorative, repairing sleep, ↑GH
In first half of the night
Declines rapidly
Declines from 50% at full term to stable 25% in adulthood
Chronic inability to obtain the necessary amount of sleep to maintain
adequate daytime behaviour
Depress REM sleep and delta sleep
‘rebound effect’ – there is a marked and immediate ↑ in the quantity
of REM sleep – as if to catch up
They have strong visual components & are seen during REM sleep
PGO spikes (pontine-geniculo-occipital)
They shut it off – maybe to stop us acting out our dreams
They are associated with intense feelings of fear & are a non-REM
phenomena
17
What is Somnambulism
When does somnambulism occur
What is Narcolepsy
What stage of sleep are narcoleptics
most likely to enter
What causes narcolepsy
What happens to the cerebral cortex if it
is left to itself
What is a major area of the brain that
controls arousal
What is the ARAS
Where does the ARAS receive sensory
input from, where does it connect to
What happens if you stimulate the ARAS
What happens to the ARAS for sleep
Where is it thought that the sleep centres
in the brain are
What are cycles of S→D & D→S due to
What is the GTF
What does the GTF consist of
What happens in GTF cells
How does the GTF affect the cortex
Why do cholinesterase inhibitors ↑ the
duration of REM sleep
What is the locus coeruleus (LC)
What is the function of the locus
coeruleus
How does the LC affect sleep
What sort of rhythm does sleep show
Where is the ‘master clock’ for biological
rhythms
What happens to sleep if the SCN is
destroyed
Limbic System
What are the limbic system & the
hypothalamus responsible for
What happens if you electrically stimulate
a reward area
What happens if you stimulate a
punishment area
What is the motivation to learn
What are psychoses
What is schizophrenia
What is schizophrenia characterised by
(symptoms
Sleep walking
Exclusively in non-REM sleep, mainly in stage 4 sleep
An irresistible urge to sleep
Directly into REM sleep
A 90% loss of orexin producing neurones, orexin stimulates
wakefulness
It reverts to slow waves (intrinsic property), so without other
influences cortical cell activity becomes synchronised – so removed
cortex from ascending inputs = S-wave sleep
The ‘Ascending reticular activating formation’(ARAS) = part of the
reticular formation in the mid-brain
Part of the reticular formation of the mid-brain
All the major sensory systems & it makes connections with the
whole of the brain & spinal cord
Arousal from sleep
It is inhibited
Brainstem, hypothalamus, preoptic area
Oscillatory activity in 2 areas of the reticular formation
Gigantocellularis tegmental field
Very large cells with long axons and dendrites that make multiple
connections throughout the brain
They exhibit oscillatory activity, bursts of APs appear just before &
during REM sleep
GTF is the origin of PGO spikes which give the visual component to
dreams
It modifies cortical activity directly through the ARAS
Neurones in the GTF are cholinergic, cholinesterase inhibitors cause
S→D sleep to occur
Another pontine area
It acts as an oscillator with the GTF, when LC cells are active GTF
are not
Opposite to GTF – causes D→S sleep to occur, causes switch from
REM sleep to S-wave sleep
Circadian = oscillations within a 24 hour period
The Suprachiasmatic nucleus (SCN) of the hypothalamus, lying just
above the optic chiasma
The circadian rhythm of sleep is lost
Instinctive & emotional behaviour, e.g. drives for thirst, sex, hunger.
It is also important in reward & punishment aspects of behaviour and
memory
Gives intense feelings of well being, euphoria and sexual arousal
Give feelings of terror, anger or pain
Learn to gain a reward or avoid a punishment
A group of disorders which represent endogenous inherent
malfunction of the brain, e.g. schizophrenia & manic depression –
relationship between behaviour and reward & punishment areas
seems to be impaired
A dissociation of the cognitive side of behaviour from the affective or
emotional side – not split personality
Bizarre delusions – or being persecuted,
Auditory hallucinations – hearing voices commenting on their actions
18
What is the action of drugs used to treat
schizophrenia
What can be the side effects of the
above drugs
What happens in disruption of
nonadrenergic pathways in the limbic
system
How can NE effect mood
How is serotonin related to mood
Memory
What is episodic memory
What is semantic memory
What is non-declarative memory
Where is non-declarative memory based
How long is immediate memory
How long is short-term memory
How long is long-term memory
What is short-term memory
Where is short-term memory stored
How is short-term memory maintained
What is retrograde amnesia
What causes retrograde amnesia
Where is the memory store
How is short-term memory converted to
long-term memory
What assesses the significance of an
event in short-term memory
What does the frontal cortex do if the
memory is considered useful
Where is memory laid down in the
cerebral cortex
What are the most powerful stimuli at
evoking long-term memories
What is the hippocampus important in
What happens if you bilateral
hippocampal damage
What is Korsakoff’s syndrome
What happens in Alzheimer’s disease
What can be used to treat Alzheimer’s
How can REM sleep be linked to memory
What happens to REM sleep in
Alzheimer’s & Korsakoff’s syndrome
How may dreaming affect memory
Sensory Systems
What is the transduction action of all
sensory receptors
What encodes the intensity of a stimulus
They interfere with dopamine transmission, mainly by blocking DA
receptors
They can interfere with the dopaminergic receptors in Basal ganglia
causing Parkinsonism
It is thought to be implicated in clinical depression
↑ ECF [NE] causes elation, ↓ ECF [NE] causes depression
Serotonin causes elation – so can treat depression by blocking
serotonin reuptake
Memory for events
Memory for words, rules and language
Relates to reflexive skills
Cerebellum
Few 100ms → 20 secs
1 sec → a few hours
30 mins → decades, centuries
An electrical phenomenon
Largely in the cerebral cortex
It needs maintained excitation from reverberating circuits
Inability to recall immediate events for up to 4 hours before loss of
consciousness
Refreshing effect (reverberating circuits) of short term memory is
interrupted
Sensory & association areas of the cortex
By a process of consolidation – this involves selective strengthening
of synaptic connection by repeated use
The frontal cortex and its association with the reward/punishment
centres in the limbic system
‘gates’ Papez circuit, so reverberating activity then continues
between the Papez circuit, frontal cortex, the sensory & association
areas until consolidation is complete
Different components in different places – e.g. visual components in
visual cortex
Olfactory stimuli
Consolidation process
You have immediate memory and intact long-term memory but are
unable to form new long-term memories
In chronic alcoholism, there is vitamin B1 deficiency & malnutrition causes mamillary body damage – the ability to consolidate memory
is impaired
There is a severe loss of cholinergic neurones throughout the brain,
including the hippocampus
Anticholinesterases - but underlying degeneration continues
Deprived of REM sleep → impairment of memory consolidation for
complex cognitive tasks
Patients have greatly reduced REM sleep – cholinergic neurones
responsible for REM sleep – dreaming may enable memory
consolidation, reinforce weak circuits
Dreaming may help forget memories that are no longer useful
Dreaming may get rid of errors (baby birds!)
All sensory receptors transducer their adequate stimulus into a
depolarisation, the receptor (generator) potential
The size of the receptor potential
19
What enables long distance transmission
How do APs encode stimulus intensity
What are the 3 types of primary afferent
fibres that mediate cutaneous
sensations, what are their properties
What is proprioception mediated by
Where do all Io afferent fibres enter the
spinal cord
What are the mechanoreceptive fibres
Where do the above fibres project
Where do the above fibres synapse
What happens to the 2nd order fibres
What are thermoreceptive & nociceptive
fibres
What happens if you damage dorsal
columns
What happens if you damage
anterolateral quadrant
Where is the ultimate termination of
semsory information
What produces the sensory homunculus
What are the effects of convergence
What is lateral inhibition
What are the effects of lateral inhibition
Physiology of pain
What usually elicits a sensation of pain
What are the two type of pain
How can somatic pain be divided up
What are pain receptors called
What are pain receptors
What are the 2 classes of pain receptors,
what are there properties
What sensations are part of ‘initial’ pain
What sensations are part of delayed pain
What nociceptors sense initial pain
What nociceptors sense delayed pain
What is the neurotransmitter released by
first order (C) neurones in pain fibres
Do pain fibres cross the mid-line
What is hyperalgesia
What is the function of substance P
Where is histamine released from
How does aspirin work
What is analgesia
Action potentials which are evoked by receptor potentials
By frequency of action potentials
Aβ – large myelinated (30-70m/s) touch, pressure, vibration
Aδ – small myelinated (5-30m/s) cold, ‘fast’ pain, pressure
C – unmyelinated fibres (0.5-2m/s) warmth, ‘slow’ pain
2 types of Io afferent fibres – Aβ & Aδ e.g. muscle spindles, GTOs
Via the dorsal root ganglia (or cranial nerve ganglia for the head)
Aα & Aβ fibres
Though ipsilateral dorsal columns
In cunate & gracile nuclei
Decussate in the brain stem & project to the reticular formation,
thalamus & cortex
Aδ & C fibres, synapse in dorsal horn, project through contralateral
spinothalamic tract to reticular formation, thalamus & cortex
Loss of touch, vibration, proprioception below lesion on ipsilateral
side
Causes loss of temperature sensation below lesion on contralateral
side
The somatosensory cortex of the postcentral gyrus
Nerve endings are grouped according to location of receptors, extent
of representation is related to the density of receptors in each
location
Saves on neurones
Reduces acuity
Underlies referred sensations
Activation of one sensory fibre causes synaptic inhibition of its
neighbours
Gives better definition of boundaries
Cleans up sensory information
A stimulus that causes or is on the verge of causing tissue damage
Somatic
Visceral
Superficial – skin
Deep = connective tissue, bones, joints, muscles
Nociceptors
Free nerve endings of primary sensory neurones
Aδ – thin myelinated, medium diameter
C – unmyelinated, small diameter
Sharp, pricking, well localised pain
Dull, intense, diffuse
Aδ
C
Substance P
Yes
Increased sensitivity to painful stimuli, the pain can last for hours
after the original stimulus is over
Causes release of substances from mast cells, which depolarise C
fibre nerve endings – causing action potentials
Mast cells & damaged cells
It is a cyclo-oxidase inhibitor, cyclo-oxidase is the enzyme that
converts arachadonic acid to prostaglandins
The selective suppression of pain without effects of consciousness
or other sensations
20
What are the 2 components of
pathiological pain
How are nociceptors different from other
receptors
Where are the cell bodies of spinal
nociceptive afferent fibres
How do nociceptive afferent fibres enter
the spinal cord, what do they then do
What type of receptor is a properties of
Aβ fibres
What type of receptors are properties of
Aδ fibres
What type of receptors are a property of
C fibres
What are the 2 main ascending pathways
to the CNS
What is the neurotransmitter released in
the dorsal horn in the spinothalamic
pathway
How many neurones are in the
spinothalamic tract
Which neurone crosses the mid-line
What does the 1st order afferent
neurones synapse with in the
Spino-reticulo-thalamic tract
What do touch fibres & pain fibres both
synapse onto
What is the ‘Gate control theory’
What activates the inhibitory
interneurones in the ‘Gate control theory’
What inhibits the inhibitory interneurones
How can the gate control theory provide
natural pain relief
What is the function of descending
pathways
Where is the Periaqueductal grey (PAG)
What does the PAG receive
What does the PAG release, what is the
effect of this
What are enkephalins/endorphins
produced by the brain
What does the above imply about
inhibitory interneurones in the gate
control system
Why is visceral pain poorly localised
What happens in referred pair
The peripheral nociceptive afferent neurone, which is activated by
noxious stimuli
The central mechanisms by which the afferent input generates a
pain sensation
They have a higher threshold, since they are normally only
activated by stimuli of noxious intensity
Dorsal root ganglia
Via the dorsal roots, ending in the grey matter of the dorsal horn,
where they give rise to the main projection pathways from the dorsal
horn to the thalamus
Mechanoreceptors
Mechanoreceptors
Nociceptors
Mechanoreceptors
Nociceptors
Thermoreceptors
Spinothalamic tract
Spino-reticulo-thalamic tract
Substance P
2
2nd order afferent neurone
An opiate interneurone
Inhibitory interneurones
It regulates the passage of impulses from the peripheral afferent
fibres to the thalamus
Descending inhibitory interneurones
Non-nociceptive input (Aα/Aβ fibres)
Nociceptor C fibre input
Rubbing the affected area stimulates the low threshold inputs onto
the inhibitory interneurone (Aα/Aβ fibres), which excites the
inhibitory interneurone, causing ↓ dorsal horn neural activity to the
CNS (thalamus)
One of the gating mechanisms that control impulse transmission in
the dorsal horn
An area of the midbrain – a small area of grey matter surrounding
the central canal
Input from many other brain regions, including the hypothalamus,
cortex & thalamus
An endogenous morphine like substance (opiod) which ↓ pain
severity = descending inhibitory pain modulation
Endogenous morphine-like substance – fits into opiod receptor
They must have opiod receptors, opiod interneurones can block pain
transmission at 2 sites, block neurotransmitter release from I o
afferent, inhibit IIo afferent
There are few receptors
Visceral pain is referred to a somatic structure from the same
dermatome, referred pain is due to convergence – there are many
more Io afferent fibres that 2nd order dorsal horn neurones
21
Why does referred pain occur
Pharmacology of pain relief
What are natural morphine-like drugs
What are semi-synthetic morphine-like
drugs
What are synthetic morphine-like drugs
What are the effects of morphine-like
drugs
What type of pain are morphine-like
drugs most effective against
What is the evidence that effects of
morphone are receptor mediated
What are the sub-types of opioid
receptors
Why does morphine work in the body
What are the mechanisms of action of
morphine
Where are the sites of action of morphine
What is the commonest cause of death in
opiod poisoning
Pharmacology of anaesthesia
How do local anaesthetics work
What are the 2 types of general
anaesthetics
What are the stages of general
anaesthesia
What are the sough after effects of
general anaesthesia
What are the unwanted effects of general
anaesthesia
What type of transmission are general
anaesthetics most effective against
Why are the target for inhalation general
anaesthetics probably not a receptor
binding site
There is somatic & visceral input onto the same dorsal horn neurone
Morphine
Codeine, heroine
Pethidine, methadone
Analgesia – against acute & chronic pain
Suppression of cough reflex (anti-tussive)
Elevation of mood (euphoria) – anxiety & agitation removed
Depression of respiration
Contraction of pupils – important diagnostic feature in overdose
Stimulates histamine release form mast cells – itching at injection
site or bronchoconstriction – don’t give to asthmatics
Increases tone in smooth muscle
Reduces smooth muscle activity e.g. gut
Dull constant pain e.g. tissue injury, inflammation & cancer (tumour
growth)
High potency
Marked stereoselectivity
Selective antagonists - naloxone
High affinity binding sites exist
Opioid receptors have been cloned
μ,δ,κ,σ – all g-protein coupled receptors, main pharmacological
effects of morphine mediated by μ receptors
Morphine taps into the endogenous signalling system for endorphins
Same as endogenous opiods) It interrupts nociceptive transmission
In the spinal cord (substantia gelatinosa)– activation of μ receptors
on central terminals of nociceptive afferent inhibits transmitter
release
In brain stem – activation of μ-receptors in PAG, stimulates
descending pathways
Respiratory depression – results in ↑ arterial Pco2 associated with a
↓ in the sensitivity of the respiratory centre to Pco2
Block voltage-dependent Na+ channels, preventing APs in afferent &
effererent axons
Inhalation anaesthetics – nitrous oxide, ether, chloroform
Intravenous anaesthetics – thiopental, ketamine
Stage I – analgesia
Stage II – excitement – dangerous stage
Stage III – surgical anaesthesia
Stage IV – medullary paralysis - lethal
Loss of sensation
Loss of consciousness
Muscle relaxation
Respiratory depression
Cardiovascular depression
Loss of reflexes
More effective against synaptic transmission than axonal conduction
– disruption of synaptic transmission in reticular formation &
thalamus
Low potency
No structure-activity relationships
No competitive antagonists
No high affinity binding sites
22
What does potency of inhalation general
anaesthetics correlate with, why?
If substances dissolve in oil are they a
good anaesthetic
What could happen if an anaesthetic
dissolved in a membrane
How do barbiturates work (intravenous)
How does ketamine work (intravenous)
Tolerance & Dependence
Describe long acting barbiturates
Name 2 long acting barbiturates
Describe shorter acting barbiturates
Name a shorter acting barbiturates
Describe very short acting barbiturates
Name a very short acting barbiturate
What do barbiturates bind to
What has to be present for barbiturates
to have an effect
What is the effect of barbiturates
What are the acute effects of barbiturates
(↑ dose down list)
What are the therapeutic uses of
barbiturates
Describe long acting benzodiazepines
Describe short acting benzodiazepines
What do benzodiazepines bind to
What is the effect of benzodiazepines
What are the acute effects of
benzodiazepines
What are the therapeutic uses of
benzodiazepines
What is Tolerance
What are the possible mechanisms of
tolerance
What are the possible mechanisms of
dispositional tolerance
What are the possible mechanisms of
pharmakodynamic tolerance
What are the 2 types of dependence
Oil:gas partition coefficient – compounds interact with something
hydrophobic to produce anaesthesia
Yes
Increased memory fluidity – unlikely
Volume expansion – explains pressure reversal of anaesthesia
Bind to GABAA receptors * potentate GABA transmission = IPSPs
Blocks NMDA receptor-gated channels, reduces glutamate
transmission (glutamate – main excitatory transmitter in brain)
Slow metabolism & excretion
Barbitone, phenobarbitone
Faster metabolism than long acting barbiturates
Pentobarbitone
Rapid redistribution from CNS to other tissues
Thiopental
Binds to subunit of GABAA receptor
GABA
Increases open time of channel when GABA binds – potentiating
GABAergic IPSPs – increasing synaptic inhibition
Anxiolytic
Hypnotic/sedation
Muscle relaxant
Causes loss of consciousness
Depresses respiratory centre – stops sensitivity to CO2
Treat epilepsy - phenobarbitone
Induce and/or maintain anaesthesia - thiopentane
Metabolised to active metabolites – diazepam
Metabolised to inactive metabolites – temazepan
Subunit of GABAA receptor
↑ affinity of GABA receptor for GABA – potentiating GABAergic
IPSPs – ↑ synaptic inhibition
Anxiolytic
Hypnotic/sedation
Muscle relaxant
Anticonvulsant
Causes loss of consciousness
Relive anxiety
Promote sleep
Induce basal anaesthesia - diazepam
Treat some types of epilepsy - diazepam
Reduced responsiveness to a drug caused by previous
administration – start needing higher concentrations to get same
effect
Dispositional – less drug reaches the active site
Pharmacodynamic – site of action is less affected by the drug
↓ rate of absorption
↑ rate of metabolism to inactive metabolites
↓ rate of metabolism to activate metabolites
↑ rate of excretion
Down-regulation or internalisation of receptors
Reduced signalling downstream of receptors
Caused by a physiological disorder e.g. diabetes
Drug induced dependence
23
What is drug induced dependence
caused by
What are reward properties caused y
What is the psychological component of
dependence
What is the general physiological effect
of drugs of depenedence
What is the specific effect of heroin
What is the specific effect of
amphetamines
What is the specific effect of cocaine
How can drug seeking behaviour be
reduced
What is the withdrawal phenomena
What is the withdrawal effect of
barbiturates
What is the withdrawal effect of opioids
What is the withdrawal effect of cocaine
What factors influence dependence
liability of a drug
Why is heroine very addictive
Brain death
What is a coma
What signs does a person in a coma
exhibit
What happens to sleep/wake cycles
during a coma
What can coma result from
What often happens to a person in an
irreversible coma
When does brain death occur
Why must the cause of coma be known
for a diagnosis of brain death
How long can a respirator be switched off
for to check for spontaneous respiration
How can you check cerebral & brainstem
functions
How must a brainstem death diagnosis
be made
Rewarding properties of the drug
Withdrawal phenomena after repeated use
Stimulation of central ‘reward pathways’, especially mesolimbic
dopaminergic neurones
Craving
They increase dopamine levels in the nucleus accumbens
Increases firing rate
Increases dopamine release
Inhibits dopamine uptake
Lesion of medial forebrain bundle
Dopamine receptor antagonists
Withdrawal effect is the reverse of the acute effect – happens
because of physiological adaptation to the drug effect (tolerance)
Acute effect = anticonvulsant, so withdrawal effect = convulsions
Acute effect = constipation, so withdrawal effect = diarrhoea
Acute effect = elevated mood, so withdrawal effect = depressed
mood
Strength of effect on reward centres vs strength of any aversive
effects
Strength of withdrawal symptoms
Discriminative effect of the drug
It crosses BBB quickly so there is a strong association between
heroine & reward
A severe ↓ in mental function due to structural, physiological, or
metabolic impairment of the brain
Sustained loss of the capacity for arousal even in response to
vigorous stimulation, no outward behavioural expression of any
mental function, eyes are closed
They disappear
Extensive damage to the cerebral cortex
Damage to the brainstem arousal mechanisms
Interruptions of connections between the brainstem and cortical
areas
Metabolic dysfunctions
Brain infections
Overdose of certain drugs e.g. sedatives, narcotics or ethanol
Enter a persistent vegetive state where sleep/wake cycles are
present, they can smile, cry but there is no evidence that they can
comprehend these behaviours
When the brain no longer functions and has no possibility of
functioning again
Comas caused by drug poisoning are usually reversible
10 mins – longer causes further brain damage due to lack of oxygen
No response to painful stimuli above the spinal cord
Pupils unresponsive to light
Apnea for 10 mins
Twice by 2 senior doctors within 24 hours, all brainstem reflexes
should be absent
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