Functional anatomy of cereberal hemispheres
• There are two cereberal hemispheres connected to each other by corpus callosum
• Each Cerebral Hemisphere is divided by sulci (fissures) into four main lobes: The Frontal, Parietal, Temporal and Occipital lobes.
The central sulcus separates the frontal from the parietal lobe. The parieto-occipital sulcus separates the parietal from the occipital lobe, and the lateral
sulcus (Sylvian fissure) separates the temporal from the frontal and parietal lobes.
A- In the Frontal Lobe:
Function Damage Irritation
1. Motor area (area 4): Initiation of voluntary motor activity of the Contralateral hemiplegia(usually starts as Motor jaksonian fits
opposite half of the body. monoplegia)
2. Premotor area (area 6): It shares the function of area 4. o Conteralateral hypertonia
o Fanning of toes on eliciting Babnizki
3. Area 8: concerned with voluntary conjugate Loss of conjugate eye movement to the Spasmodic movement
deviation of the eyes to the opposite side opposite side conjugate eye movement to
the opposite side
4. Broca's area (area 44): It is the motor speech area Expressive aphasia
5. Exner's area (area 45): the center for writing Agraphia
6. Pre-frontal area: higher center for memory. orientation, o Amnesia
thinking and intelligence. o Lack of personal Hygiene
o Disinterest in people and surroundings
B- In the Parietal Lobe:
Area Function Damage Irritation
sensory area (areas 1, 2 and 3) perception of the cortical sensation from the Contralateral hemianasthesia Sensory jaksonian fits
opposite half of the body.
area 39 recognition and recall of letters and numbers. Alexia
area 37 storage and recall of the ideas of speech and Apraxia & jargon aphasia
movements
C- In the Temporal Lobe:
Area Function Damage Irritation
1. Auditory sensory area (areas 41 and Concerned with hearing. Hearing is not lost as it is bilaterally Auditory hallucination
42): presented
2. Auditory psychic area (area 22): Recognition and recall of sounds. Auditory agnosia
, 3. Uncus Perception of smell. Smell is not lost as it is bilaterally presented Olfactory hallucination
D- In the Occipital Lobe:
Area Function Damage Irritation
1. Visual sensory area (area 17): reception of visual impulses Contralateral homonymous hemianopia Visual hallucination
2. Visual psychic area (areas 18 and recognition and recall of images Visual agnosia
19):
The Motor System
It consists of four components:
System Function
1. The pyramidal system (upper motor neurone) It is mainly concerned with the initiation of voluntary activity.
2. The extra-pyramidal system a- Voluntary and involuntary activity. b- Muscle tone.
3. The cerebellar system: coordination of voluntary activity.
4. The l ower motor neurone: transmission of impulses from the above systems to muscle fibers
The Pyramidal System(Upper Motor Neurone):
Area 4 (Primary motor area): The different parts of the opposite half of the body are represented in an inverted order→Corona radiata.→Internal capsule→ Brain
stem→Medulla: In its lower end, most of the fibers cross to the opposite side and descend in the spinal cord as the lateral corticospinal tract. The pyramidal fibers,
which end around the motor cranial nerve nuclei form the corticobulbar fibers which cross separately just above the level of the different nuclei. Some of the
corticobulbar fibers end around the motor cranial nerve nuclei of both sides.
Muscle tone:
• The length of any skeletal muscle is shorter than the distance between the origin& insertion. This puts the muscles in a stste of constant
stretch→→stimulates some muscle spindles which will send impulses through afferent sensory nerve to post. Root ganglion→ stimulation of
AHC→→The AHC will send impulses through the anterior root fibers to the muscle→→ This results in continuous subtetanic contraction which is
important to maintain muscle nourishment.
The muscle tone receives higher inhibitory control from pyramidal tract
• UMNL(▲tract): There is increase in muscle tone(spasticity) below level of lesion with no muscle muscle wasting except late(disuse atrophy)
• LMN: There id decrease in muscle tone (flaccidity) at the level of the lesion with early muscle wasting
Deep reflexes:
, • This is an induced local axon stretch reflex
• Tapping the tendon of a muscle by hammer→→ stretch of the whole muscle spindles→→ activation of local axone reflex(as in muscle tone) →→
contraction of the whole muscle
• The ▲tract excerts an inhibitory effect on the stretch reflex
• In UMNL: there is exaggeration of deep reflexes(hyper-reflexia) below the level of the lesion
• In LMNL: there is dimnution of deep reflexes(hyporeflexia) at the level of the lesion.
Clonus:
• Elicited only when there is severe▲tract lesion
• Induced by sudden sustained stretch of muscle tendon, resulting in series of rhythmic contractions. It stops with relief of tendon stretch. It is elicited in
ankle, patella, &wrist.
Effects of lesion (upper motor neurone lesion):
1. Paralysis or paresis of voluntary movements:
a- The distal muscles more than proximal muscles.
b- The progravity more than antigravity muscles i.e.The extensors of the upper limb more than the flexors and the flexors of the lower limb more than the
extensors.
2. Hypertonia or spasticity: Immediately after acute lesions, the paralysed muscles are flaccid (stage of neuronal shock) but within 2-3 weeks, tone
gradually returns and the muscles become ultimately hypertonic. This hypertonia is characteristically:
a- Maximum at the beginning of movement, smoothly sustained, and then suddenly lapses (clasp-knife phenomenon).
b- More marked in the antigravity muscles (flexors of upper limb and extensors of lower limb).
3. Posture:
a- The upper limb is adducted and internally rotated at shoulder, flexed and pronated at elbow, and flexed at wrist and fingers.
b- The lower limb is extended at hip and knee, and planter flexed at ankle. Consequently the gait consists of circumduction at the hip and
dragging of the foot.
4. Exaggerated tendon reflexes: In the stage of neuronal shock, tendon reflexes are weak or absent, but as this stage passes off they become
exaggerated and clonus may be elicited.
5. Loss of superficial (abdominal and cremasteric) reflexes.
6. Extensor planter response (Babinski reflex). 7. No muscle atrophy apart from slight disuse wasting.
The Lower Motor Neurone
Anatomy:
It consists of motor units, each unit consists of:
1. An anterior horn cell (AHC) in the spinal cord or a motor cranial nerve nucleus in the brain stem:
2. The axon of the nerve cell, which passes into:
a- An anterior root, a spinal nerve, a plexus and a peripheral nerve, or
, b- One of the motor cranial nerves.
3. Motor end-plates.
Effects of lesion (Lower motor neurone lesions = LMNL):
l. Paralysis or paresis of muscles supplied by the affected neurone. All types of movements, voluntary and involuntary are affected.
2. Wasting of affected muscles.
3. Hypotonia or flaccidity due to interruption of the efferent limb of the reflex arc.
4. Diminished or lost tendon reflexes. Abdominal, cremasteric and planter reflexes remain normal unless their neurones are damaged.
5. Fasiculations and fibrillations:
a- Fasiculations: They commonly occur with chronic degeneration of. anterior horn cells and consist of spontaneous contractions of the group of
muscle fibers supplied by the affected AHC. The contractions are visible through the skin.
b- Fibrillations: They common occur with more severe damage to the AHC and consist of spontaneous contractions of the individual muscle
fibers which get denervated. They are not visible through the skin and are detectable only by electromyography.
6. Trophic changes: These include dryness, cyanosis and -coldness of skin and brittleness of nails due to impaired blood supply to the affected part.
Differentiation between UMNL & LMNL
UMNL LMNL
1- Pararlysis Below the level of lesion At the level of the lesion
2- State of muscles NO wasting(except late due to muscle disuse) Early and marked wasting
3- Muscle tone Hypertonicity (spacticity) below the level of lesion) Hypotonia at the level of the lesion
4- Fasiculations Absent May be present in irritative lesions of AHC
5- Deep reflexes Hyper-reflexia below the level of the lesion Hyporeflexia at the level of the lesion
6- Pathological deep reflexes e.g patellar May be present Absent
7- Clonus May be present Absent
8- Superficial reflexes e.g.abdominal Lost if the lesion above the segmental supply of the reflex Lost if the lesion at the level of the reflex
9- Planter reflex (Babiniski) positive Planter flexion of toes(never say –ve Babiniski)
The Sensory System
Types of sensation:
Types Conveying fibers
Somatic sensations Superficial &deep sensations Somatic nerves
Visceral sensations Deep organs Autonomic system
Special sensations Smell, hearing, vision, taste Cranial nerves
• There are two cereberal hemispheres connected to each other by corpus callosum
• Each Cerebral Hemisphere is divided by sulci (fissures) into four main lobes: The Frontal, Parietal, Temporal and Occipital lobes.
The central sulcus separates the frontal from the parietal lobe. The parieto-occipital sulcus separates the parietal from the occipital lobe, and the lateral
sulcus (Sylvian fissure) separates the temporal from the frontal and parietal lobes.
A- In the Frontal Lobe:
Function Damage Irritation
1. Motor area (area 4): Initiation of voluntary motor activity of the Contralateral hemiplegia(usually starts as Motor jaksonian fits
opposite half of the body. monoplegia)
2. Premotor area (area 6): It shares the function of area 4. o Conteralateral hypertonia
o Fanning of toes on eliciting Babnizki
3. Area 8: concerned with voluntary conjugate Loss of conjugate eye movement to the Spasmodic movement
deviation of the eyes to the opposite side opposite side conjugate eye movement to
the opposite side
4. Broca's area (area 44): It is the motor speech area Expressive aphasia
5. Exner's area (area 45): the center for writing Agraphia
6. Pre-frontal area: higher center for memory. orientation, o Amnesia
thinking and intelligence. o Lack of personal Hygiene
o Disinterest in people and surroundings
B- In the Parietal Lobe:
Area Function Damage Irritation
sensory area (areas 1, 2 and 3) perception of the cortical sensation from the Contralateral hemianasthesia Sensory jaksonian fits
opposite half of the body.
area 39 recognition and recall of letters and numbers. Alexia
area 37 storage and recall of the ideas of speech and Apraxia & jargon aphasia
movements
C- In the Temporal Lobe:
Area Function Damage Irritation
1. Auditory sensory area (areas 41 and Concerned with hearing. Hearing is not lost as it is bilaterally Auditory hallucination
42): presented
2. Auditory psychic area (area 22): Recognition and recall of sounds. Auditory agnosia
, 3. Uncus Perception of smell. Smell is not lost as it is bilaterally presented Olfactory hallucination
D- In the Occipital Lobe:
Area Function Damage Irritation
1. Visual sensory area (area 17): reception of visual impulses Contralateral homonymous hemianopia Visual hallucination
2. Visual psychic area (areas 18 and recognition and recall of images Visual agnosia
19):
The Motor System
It consists of four components:
System Function
1. The pyramidal system (upper motor neurone) It is mainly concerned with the initiation of voluntary activity.
2. The extra-pyramidal system a- Voluntary and involuntary activity. b- Muscle tone.
3. The cerebellar system: coordination of voluntary activity.
4. The l ower motor neurone: transmission of impulses from the above systems to muscle fibers
The Pyramidal System(Upper Motor Neurone):
Area 4 (Primary motor area): The different parts of the opposite half of the body are represented in an inverted order→Corona radiata.→Internal capsule→ Brain
stem→Medulla: In its lower end, most of the fibers cross to the opposite side and descend in the spinal cord as the lateral corticospinal tract. The pyramidal fibers,
which end around the motor cranial nerve nuclei form the corticobulbar fibers which cross separately just above the level of the different nuclei. Some of the
corticobulbar fibers end around the motor cranial nerve nuclei of both sides.
Muscle tone:
• The length of any skeletal muscle is shorter than the distance between the origin& insertion. This puts the muscles in a stste of constant
stretch→→stimulates some muscle spindles which will send impulses through afferent sensory nerve to post. Root ganglion→ stimulation of
AHC→→The AHC will send impulses through the anterior root fibers to the muscle→→ This results in continuous subtetanic contraction which is
important to maintain muscle nourishment.
The muscle tone receives higher inhibitory control from pyramidal tract
• UMNL(▲tract): There is increase in muscle tone(spasticity) below level of lesion with no muscle muscle wasting except late(disuse atrophy)
• LMN: There id decrease in muscle tone (flaccidity) at the level of the lesion with early muscle wasting
Deep reflexes:
, • This is an induced local axon stretch reflex
• Tapping the tendon of a muscle by hammer→→ stretch of the whole muscle spindles→→ activation of local axone reflex(as in muscle tone) →→
contraction of the whole muscle
• The ▲tract excerts an inhibitory effect on the stretch reflex
• In UMNL: there is exaggeration of deep reflexes(hyper-reflexia) below the level of the lesion
• In LMNL: there is dimnution of deep reflexes(hyporeflexia) at the level of the lesion.
Clonus:
• Elicited only when there is severe▲tract lesion
• Induced by sudden sustained stretch of muscle tendon, resulting in series of rhythmic contractions. It stops with relief of tendon stretch. It is elicited in
ankle, patella, &wrist.
Effects of lesion (upper motor neurone lesion):
1. Paralysis or paresis of voluntary movements:
a- The distal muscles more than proximal muscles.
b- The progravity more than antigravity muscles i.e.The extensors of the upper limb more than the flexors and the flexors of the lower limb more than the
extensors.
2. Hypertonia or spasticity: Immediately after acute lesions, the paralysed muscles are flaccid (stage of neuronal shock) but within 2-3 weeks, tone
gradually returns and the muscles become ultimately hypertonic. This hypertonia is characteristically:
a- Maximum at the beginning of movement, smoothly sustained, and then suddenly lapses (clasp-knife phenomenon).
b- More marked in the antigravity muscles (flexors of upper limb and extensors of lower limb).
3. Posture:
a- The upper limb is adducted and internally rotated at shoulder, flexed and pronated at elbow, and flexed at wrist and fingers.
b- The lower limb is extended at hip and knee, and planter flexed at ankle. Consequently the gait consists of circumduction at the hip and
dragging of the foot.
4. Exaggerated tendon reflexes: In the stage of neuronal shock, tendon reflexes are weak or absent, but as this stage passes off they become
exaggerated and clonus may be elicited.
5. Loss of superficial (abdominal and cremasteric) reflexes.
6. Extensor planter response (Babinski reflex). 7. No muscle atrophy apart from slight disuse wasting.
The Lower Motor Neurone
Anatomy:
It consists of motor units, each unit consists of:
1. An anterior horn cell (AHC) in the spinal cord or a motor cranial nerve nucleus in the brain stem:
2. The axon of the nerve cell, which passes into:
a- An anterior root, a spinal nerve, a plexus and a peripheral nerve, or
, b- One of the motor cranial nerves.
3. Motor end-plates.
Effects of lesion (Lower motor neurone lesions = LMNL):
l. Paralysis or paresis of muscles supplied by the affected neurone. All types of movements, voluntary and involuntary are affected.
2. Wasting of affected muscles.
3. Hypotonia or flaccidity due to interruption of the efferent limb of the reflex arc.
4. Diminished or lost tendon reflexes. Abdominal, cremasteric and planter reflexes remain normal unless their neurones are damaged.
5. Fasiculations and fibrillations:
a- Fasiculations: They commonly occur with chronic degeneration of. anterior horn cells and consist of spontaneous contractions of the group of
muscle fibers supplied by the affected AHC. The contractions are visible through the skin.
b- Fibrillations: They common occur with more severe damage to the AHC and consist of spontaneous contractions of the individual muscle
fibers which get denervated. They are not visible through the skin and are detectable only by electromyography.
6. Trophic changes: These include dryness, cyanosis and -coldness of skin and brittleness of nails due to impaired blood supply to the affected part.
Differentiation between UMNL & LMNL
UMNL LMNL
1- Pararlysis Below the level of lesion At the level of the lesion
2- State of muscles NO wasting(except late due to muscle disuse) Early and marked wasting
3- Muscle tone Hypertonicity (spacticity) below the level of lesion) Hypotonia at the level of the lesion
4- Fasiculations Absent May be present in irritative lesions of AHC
5- Deep reflexes Hyper-reflexia below the level of the lesion Hyporeflexia at the level of the lesion
6- Pathological deep reflexes e.g patellar May be present Absent
7- Clonus May be present Absent
8- Superficial reflexes e.g.abdominal Lost if the lesion above the segmental supply of the reflex Lost if the lesion at the level of the reflex
9- Planter reflex (Babiniski) positive Planter flexion of toes(never say –ve Babiniski)
The Sensory System
Types of sensation:
Types Conveying fibers
Somatic sensations Superficial &deep sensations Somatic nerves
Visceral sensations Deep organs Autonomic system
Special sensations Smell, hearing, vision, taste Cranial nerves
