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Introduction
Dr Mohamed Rizk Khodair
Lecturer of neurology
o6u - Faculty of medicine
Mohamedrizk.med@o6u.edu.eg
Agenda
1- Nervous system
2- cerebral cortex and functional areas.
3- motor system pathway
4- sensory system pathway
Nervous system
The nervous system:
 The nervous system consists of the central nervous system
(CNS) and the peripheral nervous system (PNS). The CNS
includes the brain (within the skull) and spinal cord (within the
spinal canal of the vertebral column).
 The peripheral nervous system is classified either according to
the function or its site of origin from the nervous system into:
1. Cranial nerves that originate from brain stem except optic and
olfactory nerves.
2. Spinal nerves that originate from the spinal cord.
3. Autonomic nervous system.
The central nervous system is formed of 2 main parts
1. Intracranial parts
a) Cerebral cortex.
b) Brain stem.
c) Cerebellum.
1. Spinal part:
a) Spinal cord.
b) Cauda equina.
INTRACRANIAL PART
A. Cerebrum:
It consists of two cerebral hemispheres that are connected to each other by the corpus callosum and connected to the
upper part of the brainstem by two cerebral peduncles.
B. Brain Stem:
It consists of:
1. midbrain
2. pons
3. medulla oblongata
It is connected to the cerebral hemispheres by two peduncles, and to the cerebellum on either side by the superior, middle,
and inferior cerebellar peduncles.
It contains clusters of neurons (gray matter) interspersed with multiple ascending and descending fibers (white matter). The
motor nuclei of the cranial nerves are arranged in the brain stem as follows:
Cr 3 & 4 in Midbrain
Cr 5 & 6 & 7 in Pons
Cr 9 & 10 & 11 & 12 in medulla
Note: Cr 1, 2, and 8 are sensory nerves involved in specific sensations perceived in specific areas of the cerebral cortex
(They have no motor nuclei).
C. Cerebellum:
It is behind the brain stem and occupies most of the posterior cranial fossa. It deals with the balance maintenance and the
coordination of voluntary motor activity.
The lobes of the brain are composed of:
1-Outer gray matter, which is composed of nerve cells
(cerebral cortex) and contains many areas.
2- Inner white matter composed of nerve fibers that
transmit impulses to and from cells in the cerebral cortex.
3-At the base of each cerebral hemisphere, there are
several groups of nuclei located at different levels within
the white matter, which form the basal ganglia, thalamus,
subthalamic nucleus, and hypothalamus.
SPINAL PART
A. Spinal Cord:
It lies in the spinal canal & ends at the lower border of the 1st
lumbar vertebra. The lowest three segments of the spinal cord
(S3, 4, 5) are anatomically known as the conus medullaris, and
the above four segments (L4, 5, S1, 2) are anatomically known
as the epiconus.
B. Cauda Equina:
It is the collection of lumbosacral roots which fill the lower part
of the spinal canal below the lower border of L1 vertebra.
Cerebral Cortex
It consists of two cerebral hemispheres connected to each other by the corpus callosum and to the upper part
of the brain stem by two cerebral peduncles.
The surface of cerebral cortex is highly convoluted with the bulges, referred to as gyri, and the spaces
separating the gyri, called sulci.
The surface of each hemisphere is divided into 4 lobes:
 Frontal.
 Parietal.
 Temporal.
 Occipital.
Cerebral cortex
FRONTAL LOBE
A large area of ​​the frontal cortex in front of the central sulcus is primarily involved in the control of
movement on the opposite side of the body.
These areas include:
Primary motor (area 4) and premotor (area 6) cortex:
- The primary motor cortex is in the precentral gyrus, immediately anterior to the central sulcus.
- It contains an orderly detailed map of the skeletal muscles of the contralateral side of the body.
- representation of the body upside-down, with head, neck, upper limb, and trunk represented on the lateral aspect
of the hemisphere, and pelvis and lower limb represented medially.
- Lesions in this area lead to: Contralateral spastic paresis (region depends on the affected part of the brain
(homunculus).
The body representation in motor and sensory areas
Frontal eye field (area 8):
- located in front of the motor cortex
- It is the center of the horizontal line of sight on the contralateral side.
Lesions in this area lead to: Inability to perform spontaneous eye movements on the contralateral side.
- Because the activity of the intact frontal eye field in the opposite cortex would also be unopposed after such a
lesion, the result is conjugate slow deviation of the eyes toward the side of the lesion.
Prefrontal cortex:
- The prefrontal cortex located in front of the premotor area and represents about a quarter of the entire cerebral
cortex in the human brain.
- This area of the brain helps us plan and organize our thoughts and emotions.
Lesions in this area lead to: Frontal lobe syndrome:
1. Mentality, personality & behavioral changes: lack of attention & judgement, apathy (severe emotional
indifference), inappropriate social behavior and lack of personal hygiene, ending in dementia.
2. Reappearance of primitive reflexes as infantile suckling or grasp reflexes that are suppressed in adults
(disinhibition).
Broca’s area (area 44):
 It is the motor center for speech in the dominant hemisphere for language, which is usually the left hemisphere.
Lesions in this area lead to:
- Broca's (Expressive, non-fluent) aphasia → difficulty in piecing together words to produce expressive speech with
impaired repetition and intact comprehension (can understand written and spoken language but say almost
nothing).
Exner’s area (area 45):
- Its center of writing, adjacent to area 44 in Left hemisphere
- Lesion leading to Agraphia the patient cannot express his ideas in written words.
PARIETAL LOBE
The parietal lobe begins with the postcentral gyrus, just behind the central sulcus.
Primary somatosensory cortex (area 3, 1, 2):
- Lies in the postcentral gyrus.
- Like primary motor cortex, there is similar somatotopic representation of the body upside-down, with head, neck,
upper limb, and trunk represented on the lateral aspect of the hemisphere, and pelvis and lower limb represented
medially.
Function: perception of cortical sensation from the contralateral side of the body.
Lesions in this area lead to:
Contralateral loss of all somatic sensations (region depends on area of homunculus affected).
Posterior parietal association cortex:
Just posterior to the somatosensory areas, including:
A. Superior parietal lobule (area 5, 7):
Function: The superior parietal lobule is involved in spatial orientation, receiving, and integrating
visual as well as sensory input which is important for body image formation, the perception of the
body and its position in space.
Lesions in this area lead to:
 Astereognosia: The person has difficulty recognizing objects by touch because their brain doesn't
properly integrate visual and somatos`ensory input.
 Asomatognosia
B) Angular gyrus (Areas 39, 40):
• Domnint hemisphere , it concerned with reading , recognition and recall of letter and
numbers
• Lesion leading to alexia the patient who could read before the lesion, unable to do so.
C)Supramarginal gyrus 37:
• its dominant hemisphere its concerned with storage and recall of Idea of speech and
complex voluntary motor activity
• Lesion leading to jargon aphasia (word salad) & apraxia :inability to perform complex
voluntary motor activity in absence of paralysis, incoordination or sensory loss
TEMPORAL LOBE
Primary auditory cortex (areas 41, 42):
Function: auditory sensory area. Lesions in this area lead to:
 Slight hearing loss but not deafness as hearing is bilaterally represented.
Auditory associative area (area 22):
Function: recognition & recall of sounds. Lesions in this area lead to:
 Auditory agnosia: Patients hear but do not understand (recognize) what they are hearing.
Wernicke's area:
Function: It is the cortical area that functions in language comprehension.
Lesions in this area lead to: Wernicke's (Fluent) aphasia.
o Cause: lesion in Wernicke's area in the temporal lobe or in the parietal lobe.
o Findings: Patient cannot understand any form of language, speech is fast and fluent, but not comprehensible
(word salad) with poor repetition.
OCCIPITAL LOBE
Primary visual cortex (area 17):
Function: perception of visual images. Lesions in this area lead to:
- A unilateral lesion inside area 17 results in a contralateral homonymous hemianopia with macular sparing (because of
dual blood supply from both the posterior and middle cerebral arteries).
- Usually caused by blockage of a branch of the posterior cerebral artery.
Visual associative area (areas 18, 19):
Function: integrates complex visual input from both hemispheres for visual processing.
Lesions in this area lead to: Alexia Without Agraphia:
 A principal “higher-order” deficit associated with occipital lobe damage is alexia without agraphia (or pure word
blindness).
 The patient cannot read at all. But they can write. This is another example of disconnect syndrome, where information
from the occipital lobe is not available to the parietal or frontal lobes to understand or express what is being seen.
Motor system
THE MOTOR SYSTEM
1) The Pyramidal System (U.M.N.):
- It originates in the motor area (4) and premotor area (6) of the frontal lobe and terminates at the anterior horn cells (A.H.C.) of the
different levels of the spinal cord.
- It supplies the contralateral side of the body.
1) The Extrapyramidal System:
- It originates from centers situated at various levels of C.N.S. mainly the Basal Ganglia.
- It controls the contralateral side of the body.
1) The Cerebellar System:
- It is composed of the Neo-cerebellum, Archi-cerebellum & Paleo-cerebellum. It coordinates the movements of the same side
of the body.
1) The Lower Motor Neuron (L.M.N.)
- It is formed of Anterior Horn Cells and peripheral motor nerves (which transmit the motor impulses to the voluntary muscles).
The motor system consists of 4 main components:
Lower Motor
Neuron
Pyramidal System
Upper Motor Neuron
Extrapyramidal
System
Cerebellar System
Voluntary innervation of skeletal muscle For a
voluntary muscle to move, it should receive a
nerve impulse passing through 2 main
neurons:
1- Upper motor neuron (UMN).
2-Lower motor neuron (LMN).
Upper motor neuron (lateral corticospinal tract,
pyramidal tract):
- The voluntary motor impulse originates mainly in the large pyramidal cells (Betz cells) of the motor area (area 4) and to
a lesser extend in the cells of the premotor area (area 6).
- The axons of these cells descend in the depth of the cerebral hemisphere in the corona radiata to pass in the internal
capsule (genu & posterior limb) and continue their descend in the midbrain, pons, and medulla.
- In the lower medulla, the fibers of corticospinal tract decussate to descend in the white matter on the opposite side of
the spinal cord.
- This pathway starting from the cells of the cerebral cortex down to the spinal cord is known as the pyramidal tract or
lateral corticospinal tract.
- The corticospinal tract descends the full length of the brain stem in the lateral part of the white matter and as it descends,
axons leave the tract and enter the gray matter of the ventral horn to synapse on lower motor neuron.
- The fibers of the pyramidal tract terminate at different levels of the AHCs of the spinal cord.
Anterior horn cells or (α-motor neurons), are a special type of nerve cells that are present in the anterior horn of
the H-shaped gray matter in the spinal cord. These cell bodies are found at all segments of the spinal cord and
are mainly concentrated in the cervical and lumbosacral enlargements. They receive voluntary movement
impulses from the pyramidal tract (UMN). Their axons exit from the spinal cord as the anterior roots.
NOTE: The motor nuclei of the cranial nerves are similar in function to the AHCs as they form the cell bodies of the LMN
of the cranial nerves, thus lesion of a cranial nerve nuclei, like lesion of an AHC is a LMN lesion.
Peripheral motor nerve: carrying the motor impulse from AHCs to the voluntary muscle.
Lesions of UMN (corticospinal tract)
Lesions of UMN (corticospinal tract)
- Above the pyramidal decussation weakness is seen in muscles on the contralateral side of the body below the
level of the lesion.
- Below the pyramidal decussation ipsilateral muscle weakness below the level of the lesion.
- UMNL always below the level due to deprivation of LMN below the level of the lesion from UMN innervation.
Causes: Hemorrhage, Thrombosis, Multiple sclerosis, Traumatic brain injury…
Lesions of LMN
- A lesion to any part of a lower motor neuron will result in an ipsilateral muscle weakness at
the level of the lesion.
Causes: The most common causes of lower motor neuron injuries are trauma to peripheral
nerves that serve the axons, and viruses that selectively attack AHCs. (Poliomyelitis, DM, B12
deficiency, Myasthenia Gravis, ..)
Any lesion of the motor system (either UMN or LMN) in spinal cord will result in ipsilateral
muscle weakness (LMN at the level, UMN below the level).
Muscle tone
- This is a spontaneous local axon stretch reflex.
- The length of a skeletal muscle is less than the distance
between its origin and insertion, so the muscle is always
slightly stretched.
- Stretching stimulates several muscle spindles, sending
excitatory impulses to AHC via sensory afferents and
dorsal roots.
- Excited AHC sends motor impulses to the muscle via
the anterior root and efferent motor nerves.
- This result in continuous reflex sub-tetanic
contraction of the muscle, this constitutes the
muscle tone which is important for the
nourishment of the muscles & the posture of the
body.
The muscle tone receives higher control, mainly inhibitory, through the pyramidal & extrapyramidal
systems, therefore:
- - Loss of inhibition of the intact reflex arc leading to increased muscle tone (hypertonia) below the level of the lesion
with no wasting of the muscle.
- - Hypertonia in pyramidal tract lesion (UMNL) is called spasticity, but hypertonia in extrapyramidal lesion (basal
ganglia lesion) is called rigidity (we will talk about it later in parkinsonism).
- - Interruption of the reflex arc due to LMNL leading to decreased muscle tone (flaccidity) at the level of the lesion, with
wasting of the muscles.
Spasticity Rigidity
Due to pyramidal tract lesion (UMNL) Due to extra-pyramidal lesion
Velocity -dependent hypertonia.
Initial (or near the middle) resistance then releases (clasp entire
movement)
lead pipe or Cogwheels (interrupted by tremor).
Specific distribution of hypertonia
Specific distribution of hypertonia; affecting:
-Flexors (i.e., more resistance to extension) pronator & adductors of
upper limb.
- Extensors (i .e., more resistance to flexion); adductors & ankle
plantar flexors of Lower limb.
(unidirectional).
Equal increase in tone in the flexors
and extensors (bidirectional)
Easier to feel with rapid movements or quick jerk (spastic catch) Easier to feel with slower movements
In hemiplegic, quadriplegic, monoplegia, paraplegic distribution. Usually affects limbs and trunk, symmetrical or asymmetrical,
± hemi-distribution
Associated with other UMN signs (weakness, increase
DTRs, clonus, extensor plantar response, circumduction
or scissoring gait).
Associated with other extrapyramidal signs such as
bradykinesia, tremor, shuffling gait ).
Reflex innervation of skeletal muscle
- This is an induced local axon stretch reflex.
- It is induced by tapping the muscle tendon with a hammer.
This tap stretches the muscle by simultaneously stimulating all
muscle spindles (sensory receptors of skeletal muscle stretch
reflexes) and activating the local axon reflex (as in muscle
tone), resulting in a brief contraction of the muscle.
- The pyramidal system also exerts an inhibitory effect on this
stretch reflex, therefore:
UMNL: leads to exaggeration of deep reflexes (HYPERREFLEXIA)
below the level of the lesion.
LMNL: leads to diminution of deep reflexes (HYPOREFLEXIA) at
the level of the lesion
Clinical reflexes
Afferent limb: muscle sensory neuron (muscle spindle).
Efferent limb: lower motor neuron.
Upper motor neuron lesion & Lower motor neuron lesion
UMNL LMNL
Site of Lesion Brain and spinal cord.
(Above the AHCs)
AHCs, Nerves and muscles
Distribution of
weakness
Distal > proximal
Abbuctor > adductor
UL: extensor > flexor (progravity more than antigravity)
LL: flexor > extensor (progravity more than antigravity)
Myopathy : proximal > distal
Neuropathy: distal > proximal
Paralysis Spastic paralysis or weakness
(Clasp knife spasticity)
Flaccid paralysis or weakness.
Deep Reflexes Hyper-reflexia (brisk DTRs) below the level. Hypo or areflexia at the level.
State of Muscle No muscle wasting & if present it is late due to disuse atrophy. Early and marked muscle wasting due to loss of muscle tone.
Fasciculations Absent fasciculation. Fasciculations are present: (twitches or contractions of groups
of muscle fibers that may produce a twitch visible on the skin)
may be present due to irritation of AHCs.
Abdominal Reflexes Absent (Depending on the involved spinal level) Present
Planter Reflex
(Babinski)
+ Babinski sign (dorsiflexion of the big toe and fanning of the other
toes).
Babinski (planter) reflex is a primitive reflex in infants, normally
disappear within 1st year of life, so the presence of this reflex in
adults signify a UMNL.
Normal planter response.
Planter flexion
Muscle Tone Hypertonia (Spasticity) below the level of the lesion. Hypotonia (Flaccidity) AT the level of the lesion.
Ipsilateral or
Contralateral
Affection
UMNL will result in spastic paralysis that may be ipsilateral
(anywhere in the spinal cord will result in an ipsilateral lesion) or
contralateral (anywhere above the decussation of the pyramids will
result in contralateral lesion)
LMNL will result in flaccid paralysis that is always ipsilateral (no
crossing) and at the level of the lesion only (because the LMN at
other different levels are intact).
UMNL always below the level due to deprivation of LMN below the
level of the lesion from UMN innervation.
Sensory system
Types of sensation
General sensation
A. Somatic :
1- superficial
2- propioception (Deep)
3- cortical
B. Visceral
Special sensation
A. Smell
B. Taste
C. Vision
Sensory Neuronal system
All somatic sensation passes through 3 order neurons from sensory receptors to reach
the cortical sensory area of the opposite side:
o The cell bodies of 1st order neuron are always in the dorsal root ganglion.
o The cell of 2nd order neuron varies according to the type of sensation. The axons of the
2nd neuron crosses in the midline and is carried in a tract in the CNS.
o The cell of 3rd order neuron is the thalamus of the opposite side. The axons of the 3rd
neuron project to primary somatosensory cortex.
Anterolateral (spinothalamic tract) pathway
Lateral spinothalamic → carry pain and temperature sensation.
Anterior spinothalamic → carry crude touch and pressure sensation.
 The 1st order neuron: It is the cell of the dorsal root ganglion which
enter the spinal cord through dorsal root fibers, the axons of the 1st
order neuron ascend a couple of segments forming Lissauer's tract
and relays (synapse) in the dorsal horn of the grey matter.
 The 2nd order neuron: It is the cell bodies that are located in the
dorsal horn of the grey matter (spinal cord), the axons of the 2nd
neuron crosses to the opposite side through the ventral white
commissure just below the central canal of the spinal cord and
coalesce to form the spinothalamic tract, the axons ascend the entire
length of the spinal cord through spinothalamic tract then in brain
stem to terminate on the cells of the ventral posterolateral (VPL)
nucleus of the thalamus.
 The 3rd order neuron: start in the cells of the ventral posterolateral
(VPL) nucleus of the thalamus, then its axons pass through the
posterior limb of the internal capsule conducting the impulse to the
cortical sensory area in the parietal lobe.
Lesion of the Spinothalamic Tract
Lesions of spinothalamic tract in the spinal cord or brain stem will result in contralateral loss of pain and
temperature because the 2nd order neuron crosses almost immediately as they enter the spinal cord.
DORSAL COLUMN – Medial Lemniscus Pathway
It transmits sensory information for fine touch, proprioception (joint position
sensation), vibratory and pressure sensation.
• The 1st order neuron is the cell of the dorsal root ganglion that enter the spinal cord via
dorsal root fibers, then the axons of the 1st order neuron ascend in the gracile &
cuneate tracts within the dorsal column on the same side to relay in the gracile &
cuneate nuclei in the medulla:
Gracile Tract carries fibers from lower 1/2 of body and lies medially (Below
T7).
Cuneate Tract: carries fibers from upper 1/2 of body and lies laterally
(Above T7).
• The 2nd order neuron: from the cell of the gracile & cuneate nuclei in the lower
medulla, the axons of the 2nd neuron cross to the opposite side and ascend through
the brain stem in the medial lemniscus. Fibers of the medial lemniscus terminate on
the cells of the ventral posterolateral (VPL) nucleus of the thalamus.
• The 3rd order neuron: start in the cells of the ventral posterolateral (VPL) nucleus of
the thalamus, then its axons pass through the posterior limb of the internal capsule
conducting the impulse to the cortical sensory area in the parietal lobe.
Lesion of the dorsal column
Lesion of the dorsal column - medial lemniscus pathway in any part along the entire length of the spinal cord will result
in ipsilateral loss of vibratory and proprioceptive sensation and below the lesion, while lesion in brain stem or above
(after the 2nd order neuron crosses) will result in contralateral loss below the level of the lesion.
Any lesion along the entire length of the spinal cord will result in
Contralateral sign
1
Ipsilateral signs
2
Ipsilateral
motor signs
(UMNL signs
below the
lesion and
LMNL signs at
the level of the
lesion).
Ipsilateral loss
of vibratory
and
proprioceptiv
e sensations
below the level
of the lesion.
Contralateral loss of
pain and temperature
below the lesion.
After going through all spinal cord neural pathways, you should know:
Cortical sensations
 These are a mixture of refined superficial & deep sensations arriving
to the Thalamus via 1st and 2nd order neurons & conducted from the
thalamus via the 2nd order neuron to the cortical sensory area (1,2,3)
in the parietal lobe.
They are a group of interpretative sensory functions that depend on the analysis and integration of all the
somatosensory sensations by the parietal lobes to provide discrimination. All sensory pathways must be
intact to elicited cortical sensations. These are:
a. Stereognosis: The ability to recognize and identify objects by feeling them. Its absence is termed
astereognosis.
b. Graphesthesia: The ability to recognize symbols written on the skin. Its absence is termed graphanesthesia.
c. Two-point discrimination: The ability to recognize simultaneous stimulation by two blunt points. It is
measured by the distance between the points required for recognition.
d. Touch localization (topognosis): The ability to localize stimuli to parts of the body. Topagnosia is the
absence of this ability.
e. Double simultaneous stimulation: The ability to perceive a sensory stimulus when corresponding areas on
the opposite side of the body are stimulated simultaneously. Loss of this ability is termed sensory extinction
Pattern of sensory loss
Thank you
Mohamedrizk.med@o6u.edu.eg

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introduction to neurology (nervous system, areas, motor and sensory systems)

  • 1. Introduction Dr Mohamed Rizk Khodair Lecturer of neurology o6u - Faculty of medicine Mohamedrizk.med@o6u.edu.eg
  • 2. Agenda 1- Nervous system 2- cerebral cortex and functional areas. 3- motor system pathway 4- sensory system pathway
  • 4. The nervous system:  The nervous system consists of the central nervous system (CNS) and the peripheral nervous system (PNS). The CNS includes the brain (within the skull) and spinal cord (within the spinal canal of the vertebral column).  The peripheral nervous system is classified either according to the function or its site of origin from the nervous system into: 1. Cranial nerves that originate from brain stem except optic and olfactory nerves. 2. Spinal nerves that originate from the spinal cord. 3. Autonomic nervous system.
  • 5. The central nervous system is formed of 2 main parts 1. Intracranial parts a) Cerebral cortex. b) Brain stem. c) Cerebellum. 1. Spinal part: a) Spinal cord. b) Cauda equina.
  • 6. INTRACRANIAL PART A. Cerebrum: It consists of two cerebral hemispheres that are connected to each other by the corpus callosum and connected to the upper part of the brainstem by two cerebral peduncles. B. Brain Stem: It consists of: 1. midbrain 2. pons 3. medulla oblongata It is connected to the cerebral hemispheres by two peduncles, and to the cerebellum on either side by the superior, middle, and inferior cerebellar peduncles. It contains clusters of neurons (gray matter) interspersed with multiple ascending and descending fibers (white matter). The motor nuclei of the cranial nerves are arranged in the brain stem as follows: Cr 3 & 4 in Midbrain Cr 5 & 6 & 7 in Pons Cr 9 & 10 & 11 & 12 in medulla Note: Cr 1, 2, and 8 are sensory nerves involved in specific sensations perceived in specific areas of the cerebral cortex (They have no motor nuclei). C. Cerebellum: It is behind the brain stem and occupies most of the posterior cranial fossa. It deals with the balance maintenance and the coordination of voluntary motor activity.
  • 7. The lobes of the brain are composed of: 1-Outer gray matter, which is composed of nerve cells (cerebral cortex) and contains many areas. 2- Inner white matter composed of nerve fibers that transmit impulses to and from cells in the cerebral cortex. 3-At the base of each cerebral hemisphere, there are several groups of nuclei located at different levels within the white matter, which form the basal ganglia, thalamus, subthalamic nucleus, and hypothalamus.
  • 8. SPINAL PART A. Spinal Cord: It lies in the spinal canal & ends at the lower border of the 1st lumbar vertebra. The lowest three segments of the spinal cord (S3, 4, 5) are anatomically known as the conus medullaris, and the above four segments (L4, 5, S1, 2) are anatomically known as the epiconus. B. Cauda Equina: It is the collection of lumbosacral roots which fill the lower part of the spinal canal below the lower border of L1 vertebra.
  • 9. Cerebral Cortex It consists of two cerebral hemispheres connected to each other by the corpus callosum and to the upper part of the brain stem by two cerebral peduncles. The surface of cerebral cortex is highly convoluted with the bulges, referred to as gyri, and the spaces separating the gyri, called sulci. The surface of each hemisphere is divided into 4 lobes:  Frontal.  Parietal.  Temporal.  Occipital.
  • 11.
  • 12. FRONTAL LOBE A large area of ​​the frontal cortex in front of the central sulcus is primarily involved in the control of movement on the opposite side of the body. These areas include: Primary motor (area 4) and premotor (area 6) cortex: - The primary motor cortex is in the precentral gyrus, immediately anterior to the central sulcus. - It contains an orderly detailed map of the skeletal muscles of the contralateral side of the body. - representation of the body upside-down, with head, neck, upper limb, and trunk represented on the lateral aspect of the hemisphere, and pelvis and lower limb represented medially. - Lesions in this area lead to: Contralateral spastic paresis (region depends on the affected part of the brain (homunculus).
  • 13. The body representation in motor and sensory areas
  • 14. Frontal eye field (area 8): - located in front of the motor cortex - It is the center of the horizontal line of sight on the contralateral side. Lesions in this area lead to: Inability to perform spontaneous eye movements on the contralateral side. - Because the activity of the intact frontal eye field in the opposite cortex would also be unopposed after such a lesion, the result is conjugate slow deviation of the eyes toward the side of the lesion.
  • 15. Prefrontal cortex: - The prefrontal cortex located in front of the premotor area and represents about a quarter of the entire cerebral cortex in the human brain. - This area of the brain helps us plan and organize our thoughts and emotions. Lesions in this area lead to: Frontal lobe syndrome: 1. Mentality, personality & behavioral changes: lack of attention & judgement, apathy (severe emotional indifference), inappropriate social behavior and lack of personal hygiene, ending in dementia. 2. Reappearance of primitive reflexes as infantile suckling or grasp reflexes that are suppressed in adults (disinhibition).
  • 16. Broca’s area (area 44):  It is the motor center for speech in the dominant hemisphere for language, which is usually the left hemisphere. Lesions in this area lead to: - Broca's (Expressive, non-fluent) aphasia → difficulty in piecing together words to produce expressive speech with impaired repetition and intact comprehension (can understand written and spoken language but say almost nothing). Exner’s area (area 45): - Its center of writing, adjacent to area 44 in Left hemisphere - Lesion leading to Agraphia the patient cannot express his ideas in written words.
  • 17. PARIETAL LOBE The parietal lobe begins with the postcentral gyrus, just behind the central sulcus. Primary somatosensory cortex (area 3, 1, 2): - Lies in the postcentral gyrus. - Like primary motor cortex, there is similar somatotopic representation of the body upside-down, with head, neck, upper limb, and trunk represented on the lateral aspect of the hemisphere, and pelvis and lower limb represented medially. Function: perception of cortical sensation from the contralateral side of the body. Lesions in this area lead to: Contralateral loss of all somatic sensations (region depends on area of homunculus affected).
  • 18. Posterior parietal association cortex: Just posterior to the somatosensory areas, including: A. Superior parietal lobule (area 5, 7): Function: The superior parietal lobule is involved in spatial orientation, receiving, and integrating visual as well as sensory input which is important for body image formation, the perception of the body and its position in space. Lesions in this area lead to:  Astereognosia: The person has difficulty recognizing objects by touch because their brain doesn't properly integrate visual and somatos`ensory input.  Asomatognosia
  • 19. B) Angular gyrus (Areas 39, 40): • Domnint hemisphere , it concerned with reading , recognition and recall of letter and numbers • Lesion leading to alexia the patient who could read before the lesion, unable to do so. C)Supramarginal gyrus 37: • its dominant hemisphere its concerned with storage and recall of Idea of speech and complex voluntary motor activity • Lesion leading to jargon aphasia (word salad) & apraxia :inability to perform complex voluntary motor activity in absence of paralysis, incoordination or sensory loss
  • 20. TEMPORAL LOBE Primary auditory cortex (areas 41, 42): Function: auditory sensory area. Lesions in this area lead to:  Slight hearing loss but not deafness as hearing is bilaterally represented. Auditory associative area (area 22): Function: recognition & recall of sounds. Lesions in this area lead to:  Auditory agnosia: Patients hear but do not understand (recognize) what they are hearing. Wernicke's area: Function: It is the cortical area that functions in language comprehension. Lesions in this area lead to: Wernicke's (Fluent) aphasia. o Cause: lesion in Wernicke's area in the temporal lobe or in the parietal lobe. o Findings: Patient cannot understand any form of language, speech is fast and fluent, but not comprehensible (word salad) with poor repetition.
  • 21. OCCIPITAL LOBE Primary visual cortex (area 17): Function: perception of visual images. Lesions in this area lead to: - A unilateral lesion inside area 17 results in a contralateral homonymous hemianopia with macular sparing (because of dual blood supply from both the posterior and middle cerebral arteries). - Usually caused by blockage of a branch of the posterior cerebral artery. Visual associative area (areas 18, 19): Function: integrates complex visual input from both hemispheres for visual processing. Lesions in this area lead to: Alexia Without Agraphia:  A principal “higher-order” deficit associated with occipital lobe damage is alexia without agraphia (or pure word blindness).  The patient cannot read at all. But they can write. This is another example of disconnect syndrome, where information from the occipital lobe is not available to the parietal or frontal lobes to understand or express what is being seen.
  • 23. THE MOTOR SYSTEM 1) The Pyramidal System (U.M.N.): - It originates in the motor area (4) and premotor area (6) of the frontal lobe and terminates at the anterior horn cells (A.H.C.) of the different levels of the spinal cord. - It supplies the contralateral side of the body. 1) The Extrapyramidal System: - It originates from centers situated at various levels of C.N.S. mainly the Basal Ganglia. - It controls the contralateral side of the body. 1) The Cerebellar System: - It is composed of the Neo-cerebellum, Archi-cerebellum & Paleo-cerebellum. It coordinates the movements of the same side of the body. 1) The Lower Motor Neuron (L.M.N.) - It is formed of Anterior Horn Cells and peripheral motor nerves (which transmit the motor impulses to the voluntary muscles). The motor system consists of 4 main components: Lower Motor Neuron Pyramidal System Upper Motor Neuron Extrapyramidal System Cerebellar System
  • 24. Voluntary innervation of skeletal muscle For a voluntary muscle to move, it should receive a nerve impulse passing through 2 main neurons: 1- Upper motor neuron (UMN). 2-Lower motor neuron (LMN).
  • 25. Upper motor neuron (lateral corticospinal tract, pyramidal tract): - The voluntary motor impulse originates mainly in the large pyramidal cells (Betz cells) of the motor area (area 4) and to a lesser extend in the cells of the premotor area (area 6). - The axons of these cells descend in the depth of the cerebral hemisphere in the corona radiata to pass in the internal capsule (genu & posterior limb) and continue their descend in the midbrain, pons, and medulla. - In the lower medulla, the fibers of corticospinal tract decussate to descend in the white matter on the opposite side of the spinal cord. - This pathway starting from the cells of the cerebral cortex down to the spinal cord is known as the pyramidal tract or lateral corticospinal tract. - The corticospinal tract descends the full length of the brain stem in the lateral part of the white matter and as it descends, axons leave the tract and enter the gray matter of the ventral horn to synapse on lower motor neuron. - The fibers of the pyramidal tract terminate at different levels of the AHCs of the spinal cord.
  • 26. Anterior horn cells or (α-motor neurons), are a special type of nerve cells that are present in the anterior horn of the H-shaped gray matter in the spinal cord. These cell bodies are found at all segments of the spinal cord and are mainly concentrated in the cervical and lumbosacral enlargements. They receive voluntary movement impulses from the pyramidal tract (UMN). Their axons exit from the spinal cord as the anterior roots. NOTE: The motor nuclei of the cranial nerves are similar in function to the AHCs as they form the cell bodies of the LMN of the cranial nerves, thus lesion of a cranial nerve nuclei, like lesion of an AHC is a LMN lesion. Peripheral motor nerve: carrying the motor impulse from AHCs to the voluntary muscle.
  • 27. Lesions of UMN (corticospinal tract) Lesions of UMN (corticospinal tract) - Above the pyramidal decussation weakness is seen in muscles on the contralateral side of the body below the level of the lesion. - Below the pyramidal decussation ipsilateral muscle weakness below the level of the lesion. - UMNL always below the level due to deprivation of LMN below the level of the lesion from UMN innervation. Causes: Hemorrhage, Thrombosis, Multiple sclerosis, Traumatic brain injury…
  • 28. Lesions of LMN - A lesion to any part of a lower motor neuron will result in an ipsilateral muscle weakness at the level of the lesion. Causes: The most common causes of lower motor neuron injuries are trauma to peripheral nerves that serve the axons, and viruses that selectively attack AHCs. (Poliomyelitis, DM, B12 deficiency, Myasthenia Gravis, ..) Any lesion of the motor system (either UMN or LMN) in spinal cord will result in ipsilateral muscle weakness (LMN at the level, UMN below the level).
  • 29. Muscle tone - This is a spontaneous local axon stretch reflex. - The length of a skeletal muscle is less than the distance between its origin and insertion, so the muscle is always slightly stretched. - Stretching stimulates several muscle spindles, sending excitatory impulses to AHC via sensory afferents and dorsal roots. - Excited AHC sends motor impulses to the muscle via the anterior root and efferent motor nerves. - This result in continuous reflex sub-tetanic contraction of the muscle, this constitutes the muscle tone which is important for the nourishment of the muscles & the posture of the body.
  • 30. The muscle tone receives higher control, mainly inhibitory, through the pyramidal & extrapyramidal systems, therefore: - - Loss of inhibition of the intact reflex arc leading to increased muscle tone (hypertonia) below the level of the lesion with no wasting of the muscle. - - Hypertonia in pyramidal tract lesion (UMNL) is called spasticity, but hypertonia in extrapyramidal lesion (basal ganglia lesion) is called rigidity (we will talk about it later in parkinsonism). - - Interruption of the reflex arc due to LMNL leading to decreased muscle tone (flaccidity) at the level of the lesion, with wasting of the muscles.
  • 31. Spasticity Rigidity Due to pyramidal tract lesion (UMNL) Due to extra-pyramidal lesion Velocity -dependent hypertonia. Initial (or near the middle) resistance then releases (clasp entire movement) lead pipe or Cogwheels (interrupted by tremor). Specific distribution of hypertonia Specific distribution of hypertonia; affecting: -Flexors (i.e., more resistance to extension) pronator & adductors of upper limb. - Extensors (i .e., more resistance to flexion); adductors & ankle plantar flexors of Lower limb. (unidirectional). Equal increase in tone in the flexors and extensors (bidirectional) Easier to feel with rapid movements or quick jerk (spastic catch) Easier to feel with slower movements In hemiplegic, quadriplegic, monoplegia, paraplegic distribution. Usually affects limbs and trunk, symmetrical or asymmetrical, ± hemi-distribution Associated with other UMN signs (weakness, increase DTRs, clonus, extensor plantar response, circumduction or scissoring gait). Associated with other extrapyramidal signs such as bradykinesia, tremor, shuffling gait ).
  • 32. Reflex innervation of skeletal muscle - This is an induced local axon stretch reflex. - It is induced by tapping the muscle tendon with a hammer. This tap stretches the muscle by simultaneously stimulating all muscle spindles (sensory receptors of skeletal muscle stretch reflexes) and activating the local axon reflex (as in muscle tone), resulting in a brief contraction of the muscle. - The pyramidal system also exerts an inhibitory effect on this stretch reflex, therefore: UMNL: leads to exaggeration of deep reflexes (HYPERREFLEXIA) below the level of the lesion. LMNL: leads to diminution of deep reflexes (HYPOREFLEXIA) at the level of the lesion Clinical reflexes Afferent limb: muscle sensory neuron (muscle spindle). Efferent limb: lower motor neuron.
  • 33. Upper motor neuron lesion & Lower motor neuron lesion UMNL LMNL Site of Lesion Brain and spinal cord. (Above the AHCs) AHCs, Nerves and muscles Distribution of weakness Distal > proximal Abbuctor > adductor UL: extensor > flexor (progravity more than antigravity) LL: flexor > extensor (progravity more than antigravity) Myopathy : proximal > distal Neuropathy: distal > proximal Paralysis Spastic paralysis or weakness (Clasp knife spasticity) Flaccid paralysis or weakness. Deep Reflexes Hyper-reflexia (brisk DTRs) below the level. Hypo or areflexia at the level. State of Muscle No muscle wasting & if present it is late due to disuse atrophy. Early and marked muscle wasting due to loss of muscle tone. Fasciculations Absent fasciculation. Fasciculations are present: (twitches or contractions of groups of muscle fibers that may produce a twitch visible on the skin) may be present due to irritation of AHCs. Abdominal Reflexes Absent (Depending on the involved spinal level) Present Planter Reflex (Babinski) + Babinski sign (dorsiflexion of the big toe and fanning of the other toes). Babinski (planter) reflex is a primitive reflex in infants, normally disappear within 1st year of life, so the presence of this reflex in adults signify a UMNL. Normal planter response. Planter flexion Muscle Tone Hypertonia (Spasticity) below the level of the lesion. Hypotonia (Flaccidity) AT the level of the lesion. Ipsilateral or Contralateral Affection UMNL will result in spastic paralysis that may be ipsilateral (anywhere in the spinal cord will result in an ipsilateral lesion) or contralateral (anywhere above the decussation of the pyramids will result in contralateral lesion) LMNL will result in flaccid paralysis that is always ipsilateral (no crossing) and at the level of the lesion only (because the LMN at other different levels are intact). UMNL always below the level due to deprivation of LMN below the level of the lesion from UMN innervation.
  • 34.
  • 36. Types of sensation General sensation A. Somatic : 1- superficial 2- propioception (Deep) 3- cortical B. Visceral Special sensation A. Smell B. Taste C. Vision
  • 37. Sensory Neuronal system All somatic sensation passes through 3 order neurons from sensory receptors to reach the cortical sensory area of the opposite side: o The cell bodies of 1st order neuron are always in the dorsal root ganglion. o The cell of 2nd order neuron varies according to the type of sensation. The axons of the 2nd neuron crosses in the midline and is carried in a tract in the CNS. o The cell of 3rd order neuron is the thalamus of the opposite side. The axons of the 3rd neuron project to primary somatosensory cortex.
  • 38. Anterolateral (spinothalamic tract) pathway Lateral spinothalamic → carry pain and temperature sensation. Anterior spinothalamic → carry crude touch and pressure sensation.  The 1st order neuron: It is the cell of the dorsal root ganglion which enter the spinal cord through dorsal root fibers, the axons of the 1st order neuron ascend a couple of segments forming Lissauer's tract and relays (synapse) in the dorsal horn of the grey matter.  The 2nd order neuron: It is the cell bodies that are located in the dorsal horn of the grey matter (spinal cord), the axons of the 2nd neuron crosses to the opposite side through the ventral white commissure just below the central canal of the spinal cord and coalesce to form the spinothalamic tract, the axons ascend the entire length of the spinal cord through spinothalamic tract then in brain stem to terminate on the cells of the ventral posterolateral (VPL) nucleus of the thalamus.  The 3rd order neuron: start in the cells of the ventral posterolateral (VPL) nucleus of the thalamus, then its axons pass through the posterior limb of the internal capsule conducting the impulse to the cortical sensory area in the parietal lobe.
  • 39. Lesion of the Spinothalamic Tract Lesions of spinothalamic tract in the spinal cord or brain stem will result in contralateral loss of pain and temperature because the 2nd order neuron crosses almost immediately as they enter the spinal cord.
  • 40. DORSAL COLUMN – Medial Lemniscus Pathway It transmits sensory information for fine touch, proprioception (joint position sensation), vibratory and pressure sensation. • The 1st order neuron is the cell of the dorsal root ganglion that enter the spinal cord via dorsal root fibers, then the axons of the 1st order neuron ascend in the gracile & cuneate tracts within the dorsal column on the same side to relay in the gracile & cuneate nuclei in the medulla: Gracile Tract carries fibers from lower 1/2 of body and lies medially (Below T7). Cuneate Tract: carries fibers from upper 1/2 of body and lies laterally (Above T7). • The 2nd order neuron: from the cell of the gracile & cuneate nuclei in the lower medulla, the axons of the 2nd neuron cross to the opposite side and ascend through the brain stem in the medial lemniscus. Fibers of the medial lemniscus terminate on the cells of the ventral posterolateral (VPL) nucleus of the thalamus. • The 3rd order neuron: start in the cells of the ventral posterolateral (VPL) nucleus of the thalamus, then its axons pass through the posterior limb of the internal capsule conducting the impulse to the cortical sensory area in the parietal lobe.
  • 41. Lesion of the dorsal column Lesion of the dorsal column - medial lemniscus pathway in any part along the entire length of the spinal cord will result in ipsilateral loss of vibratory and proprioceptive sensation and below the lesion, while lesion in brain stem or above (after the 2nd order neuron crosses) will result in contralateral loss below the level of the lesion.
  • 42. Any lesion along the entire length of the spinal cord will result in Contralateral sign 1 Ipsilateral signs 2 Ipsilateral motor signs (UMNL signs below the lesion and LMNL signs at the level of the lesion). Ipsilateral loss of vibratory and proprioceptiv e sensations below the level of the lesion. Contralateral loss of pain and temperature below the lesion. After going through all spinal cord neural pathways, you should know:
  • 43. Cortical sensations  These are a mixture of refined superficial & deep sensations arriving to the Thalamus via 1st and 2nd order neurons & conducted from the thalamus via the 2nd order neuron to the cortical sensory area (1,2,3) in the parietal lobe. They are a group of interpretative sensory functions that depend on the analysis and integration of all the somatosensory sensations by the parietal lobes to provide discrimination. All sensory pathways must be intact to elicited cortical sensations. These are: a. Stereognosis: The ability to recognize and identify objects by feeling them. Its absence is termed astereognosis. b. Graphesthesia: The ability to recognize symbols written on the skin. Its absence is termed graphanesthesia. c. Two-point discrimination: The ability to recognize simultaneous stimulation by two blunt points. It is measured by the distance between the points required for recognition. d. Touch localization (topognosis): The ability to localize stimuli to parts of the body. Topagnosia is the absence of this ability. e. Double simultaneous stimulation: The ability to perceive a sensory stimulus when corresponding areas on the opposite side of the body are stimulated simultaneously. Loss of this ability is termed sensory extinction