Neuro Science Final

NEURO SCIENCE MODULE
1st MBBS Repeat Campaign - 2019
26TH BATCH – 2015/2016

Faculty of Medical Sciences – University of Sri Jayewardenepura
1st MBBS Repeat Campaign – 26th Batch 1
Index
Physiology
1. Sensory system
2. Pain
3. Motor system and reflexes
4. Spinal cord and tracts
5. Spinal cord lesions
6. Special senses
Vision
Hearing and balance
Taste and smell
7. Cerebral blood flow
8. Blood brain barrier
9. CSF
10. Cerebellum
11. Basal ganglia
12. Hypothalamus
13. Internal capsule
14. Higher functions
15. Sleep
16. Brain death
Anatomy
1. Brain stem
2. Cranial nerves and lesions
3. Meninges, hemorrhages and cavernous sinus
4. Blood supply of the brain
5. Cerebrum sulci and gyri
6. Thalamus
7. Limbic system
8. Parasympathetic ganglia
Sensory system •Nociceptors: Cutaneous free nerve endings that respond to stimuli that are
harmful and pain and extreme temperature.
Properties of sensory receptors
1. Mechanical: - Strong pressure
•Types of sensory receptors 2. Thermal: - Extreme temperatures
3. Chemical: - Bradykinin, histamine, Acids, irritants, Prostaglandins
1. Touch
4. Polymodal: - Combination
2. Pressure
3. Temperature •Thermoreceptors: Skin has cold and heat sensitive spots.
4. Vibration
No. of cold sensitive spots >> No. of heat sensitive spots.
5. Proprioception
[Sense of joint position/ motion/ tension of muscles] 1. Warmth receptors -> C fibers
Threshold for activation = 30°C
•Sensory receptor
2. Cold receptors -> Aδ/C fibers
Transducers that convert energy (stimuli) into action potentials in sensory Inactive at 40°C
neurons Increased activity down to ≥ 4°C
If associated with non-neural cells -> sensory organs Decreased activity and inactivation up to 10°C [Has an anesthetic effect]
Functions of a receptor
Receive specific stimuli
Respond best to one form of energy
Convert external form of energy to recognizable energy
Sensory transduction
Sensory receptor stimulated
Change RMP Generator receptor potentials (GRP)
If GRP is similar or higher than threshold for stimulus
Trigger AP
[Sensory transduction occurs through changes in membrane potentials]

Generator potentials Sensation

Stimulus is given
Non propagating action potentials: - Generator potentials occur
[Magnitude depend on intensity of stimulus ∴Graded potentials]
When the magnitude of the GP reaches a certain value, ab AP is produced

at the 1st node of Ranvier Signal strength and no of Stimulus
stimulated fibers
[Frequency of AP generation is proportional to the magnitude of GP ∴ to
the intensity of stimulus.] 1. Greater stimulus ↑generator potential amplitude
↑AP frequency
Sensory coding 2. Recruitment of other sensory units
3. Presence of receptors of varying threshold
Correcting a receptor stimulus to a recognizable sensation
4 elements; Signal
intensity
1. Modality
Types of energy transmitted by the stimulus
Spatial summation Temporal summation
Receptors respond to other forms of energy but threshold is high
Adequate stimulus -> Form of energy to which a receptor is most
sensitive. Signal strength and frequency of
Stimulation
2. Localization AP
Site on body where stimulus originates
Sensory unit: -Single sensory axon and its peripheral branches.
Receptive field of sensory unit: Spatial distribution from which a 4. Duration
stimulus produces a response in that unit. Refers to time from start to end of the response in stimulus
Lateral inhibition: - Impulses from neurons closer to the stimulus
inhibits more peripheral impulses. Receptor adaptation: Prolonged, constant stimulus decreases AP frequency
Enables localization and basis of 2-point discrimination. over time.
3. Intensity
Signaled by response amplitude or frequency of AP generated
Adaptation/Desensitization
Recruitment of sensory units
Rapidly adapting
Slowly adapting When the strength of stimulus increases
receptors (Phasic)
receptors (tonic)
Activate sensory organs,
- Immediately contact with

Transmits impulses to brain as long as - Recruitment of those in surrounding area
Rapidly adapt to a
constant stimulus by stimulus is present.
decreasing frequency of Make the brain constantly aware of ↑ afferents
AP over a time. the status of the body and it’s
Ex: Pacinian surroundings.
Ex: Pain Interpretation of brain as,
↑ intensity of the sensations

Law of specific nerve endings
NOTE: Weak stimuli activate receptors with lowest threshold
The sensation evoked is that for which the receptor is specialized regardless
of the modality(how) and localization(where) along the nerve, the activity is Stronger stimuli activate receptors with highest threshold
initiated.
Law of projection
Neurological examination
Whenever a particular sensory pathway is stimulated along its course from
•2point threshold test
receptor to sensory cortex of the brain, the conscious sensation is felt by
the individual is referred to the site of receptors Tactile activity varies with parts of the body, tests integrity of Dorsal
column/ Medial lemnisci
Eg: Phantom limb
•Pallesthesia: Vibratory sensibility
- 128Hz tuning fork on finger tips/bones

- Pacinian corpuscles, dorsal columns
- Degeneration occurs in
Poorly controlled diabetes mellitus
Pernicious anemia/ B12 deficiency
Tabes dorsalis
•Stereognosis Known as “bad pain” because it persists after recovery from an injury and is often
refractory to common analgesic agents (NSAIDs and opioids)
Identifying objects by touch
Examples for chronic pain – pain in the development of an abscess, pain in severe
Intact dorsal column and primary sensory cortex and somattesthetic arthritis.
association cortex is needed.
RECEPTION OF PAIN
PAIN Takes place in free nerve endings
Mechanical and thermal stimuli – can elicit both fast and slow pains Chemical
stimuli – slow pain
DEFINITIONS OF PAIN
Chemicals like serotonin, histamine, bradykinin, lactic acid and K+ can be found in
1.An unpleasant sensory and emotional experience associated with actual or damaged tissue – they excite free nerve endings.
potential tissue damage, or described in terms of such damage.
The threshold for pain endings can be lowered by Prostaglandins and Substance P
but CANNOT stimulate the nerve endings by themselves.
2.The physical adjunct to an imperative protective reflex.
CONDUCTION OF PAIN
Definition of nociception - unconscious activity induced by a harmful stimulus TO THE CNS
applied to sense receptors.
peripheral nerves
CLASSSIFICATION OF PAIN Fast pain – In large diameter A delta fibers
Slow pain – In small diameter C fibers
A)Acute pain (physiologic)
Velocity of conduction is higher in A delta fiber.
Features
Fast pain reaches consciousness much faster – protective response takes place
1.Sudden onset , recedes during healing process
2.Experienced within about 0.1 seconds after stimulation Slow pain – appreciated later and lasts much longer than fast pain.
3.Almost confined to the skin
4.Can be precisely localized IN THE CNS
Known as “good pain” as it serves an important protective mechanism. Afferent pain fibers (A delta fibers, C fibers)
Withdrawal reflex is an expression of the protective role. posterior roots of spinal nerve
Example for acute pain - pain felt after pricking the finger with a needle. terminate in the superficial layer of posterior gray horn
B) Chronic pain (pathologic) : includes inflammatory and neuropathic pain
1.Slow pain, described as burning, throbbing pain – produced in tissue destruction

2. Experienced 1.0 second or later after stimulation.
3.Can occur in any tissue of the body.
4.Poorly localized
PATHWAY OF FAST PAIN These chemicals can either sensitize (increase responsiveness) or
directly activate nociceptors.
Cell bodies of afferent neurons in posterior gray horn
Injured cells release :
Stimulates second order neurons of lateral ST tract
1.K+ ions – depolarize nerve terminals –makes nociceptors more responsive
Immediately cross to the opposite side of the spinal cord (sensitization)
2.bradykinin and substance P – further sensitize nociceptors
Ascend to VPL nucleus of the thalamus 3.Histamine (from mast cells), serotonin and prostaglandins – sensitizes and directly
activates nociceptors.
Post Central gyrus (sensory)
4.Bradykinin – activates both A delta and C fibers, increases the synthesis and
PATHWAY OF SLOW PAIN release of prostaglandins
Also stimulates second order neurons of the lateral ST tract CLINICAL CORRELATES
Ascend with the axons of the fast-acting pain fibers Usage of NSAIDs in pain relief
Majority terminates in the reticular formation Prostaglandin E2 is released from damaged cells and causes increased sensitivity to
pain.
Prostaglandin E2 – derived from arachidonic acid - is a metabolite of cyclooxygenase
DIFFERENCE BETWEEN THE TWO PATHWAYS (COX) enzyme.
the incoming slow fibers to the spinal cord have multiple relays involving several Aspirin and other NSAIDs are non-selective inhibitors of COX
neurons in the posterior gray horn before ascending in the spinal cord thus the reduction of prostaglandins by NSAIDs alleviate pain.
This results in slow pain being poorly localized as opposed to fast pain (precisely CONTROL OF PAIN IN THE CNS
localized) whose afferent fibers ascend directly in the spinal cord. •Gating theory
WINDING UP PHENOMENON OF C FIBERS Explains the relieving of pain by massaging painful areas, applying oil, acupuncture,
Repeated arrival of noxious stimuli through C fibers in the posterior gray horn low frequency electrical stimulation of the skin.
results in an increased response of 2nd order neurons It is suggested that,
OTHER PARTS OF THE BRAIN AND THEIR FUNCTIONS IN PAIN RECEPTION at the site where the pain fiber enters the CNS, inhibition can occur by connector
neurons.
Post central gyrus – interpreting pain in relation to past experiences These connector neurons are excited by myelinated afferent fibers carrying
cingulate gyrus – interpreting the emotional aspect of pain nonpainful touch and pressure stimuli.
insular gyrus – interpreting the pain stimuli from internal organs –brings about an Therefore, excess tactile stimulation by a massage in the painful area “closes the
autonomic response. gate” for pain.
CHEMICALS INVOLVED IN PAIN (see also PAIN RECEPTION) However, when the tactile stimulation stops, the “gate reopens” and information
on painful stimuli ascend in the LSTT.
Chemical mediators are released in response to tissue damage
•Analgesia system
Causes inflammatory pain
Stimulation of the following areas in the brainstem can reduce or block sensations BASIS FOR REFERRED PAIN
of pain.
Convergence – projection theory
1. periventricular area of the diencephalon convergence of somatic and visceral pain fibers on the same second order
2. periaqueductal gray matter of the midbrain neuron
3. midline nuclei of the brainstem
Second order neurons in the dorsal horn
Fibers of the reticulospinal tract
Thalamus Somatosensory cortex
Spinal cord
Somatic and visceral neurons converge in the ipsilateral dorsal horn
Synapse on cells of pain sensation in the posterior gray column
Convergence-facilitation theory
Neurotransmitters in the analgesic system – enkephalins
The somatic nociceptive fibers normally do not activate the 2nd order neurons.
and endorphins (have morphinelike actions) Serotonin
But when visceral stimulation is prolonged
These substances act in the brain and also inhibits release of substance P in the
posterior gray column. Facilitation of somatic nerve endings
TYPES OF PAIN Somatic nerve endings now stimulate the 2nd order neurons
•Chronic pain Brain cannot determine whether the stimulus cam from the viscera or the somatic
area
Can result from nerve injury (neuropathic pain)
as occurs in Diabetic neuropathy Referred pain
toxin-induced nerve damage and ischemia
•Causalgia – a type of neuropathic pain
•HYPERALGESIA AND ALLODYNIA
Pain is often accompanied by
Hyperalgesia – an exaggerated response to a noxious stimulus

Allodynia – sensation of pain in response to a normally innocuous stimulus
Hyperalgesia and allodynia indicate inceased sensitivity to nociceptive fibers.
REFERRED PAIN
Irritation of a visceral organ can produce pain that is felt not at that site but in a
somatic structure that is some distance away from the visceral organ.
In referred pain the somatic structure that experiences the pain usually has the
same embryonic origin as the visceral structure where the pain originates from.
E.g. :-the heart and arm have the same segmental origin.
Impulses are continuously sent through afferent fibres and muscle is continuously
Motor System contracted
Monosynaptic Reflex
➢ There are contractile ends in the Intrafusal fibres which are innervated by γ
Is the simplest reflex arc including a single synapse between an afferent and an
neurons from the Ventral horn of Spinal Cord. These are under higher
efferent neuron
control and usually their discharge is reduced by the higher centers.
Stretch Reflex (Myotatic Reflex)
When γ motor neurons are stimulated
Muscle Spindle – Consists of Intrafusal fibres

Contractile units of Intrafusal fibres are stimulated
• 2/3 Nuclear Bag Fibres (two types- Static and Dynamic)
• 5 Nuclear Chain Fibres
Nuclear Bag portion is stretched
➢ Muscle is made up of
Impulses are generated in 1a endings
• Extrafusal Fibres – Muscle Contraction and Relaxtion
• Muscle Spindle – Arranged parallel to Extrafusal fibres and act as
This causes stimulation of α MNs and hence contraction of the muscle
sensory organ of Muscle Stretch
➢ Therefore, innervation by γ MNs increases Spindle Sensitivity of the

Muscle is stretched passively
muscle
➢ Anxiety causes increased discharge in γ MNs giving hyperactive tendon
Sensed by stretching of Intrafusal fibres of Muscle Spindle (Loading the Spindle) reflexes
Afferent fibres send impulses to the α Motor Neuron innervating the Extrafusal ➢ Reciprocal Innervation – When a stretch reflex occurs, the antagonizing
Fibres of the Muscle
muscles are relaxed
• 1a nerve endings transmit from all Nuclear bag and Nuclear chain ifbres
Eg – Bicep muscle is stretched passively
• 2 nerve endings transmit donot transmit from dynamic nuclear bag fibres
(but transmit from all other fibres)
Impulses are generated in 1a and 2 endings of muscle spindles in Biceps
Synapse between the afferent fibres and α Motor neuron of that muscle
Collaterals from those afferent fibres synapse with an inhibitory neuron in spinal
cord which synapses with the α MNs of Triceps (Antagonist) muscle
Impulses sent through α Motor neuron
Hence stimulation of intrafusal fbres in Biceps inhibit contraction of Triceps
Contraction of Extrafusal Fibres and hence the Muscle
If the stretch is maintained
Inverse Stretch Reflex When the ankle is passively dorsiflexed, stretch reflex occurs in the
muscles involved in plantar flexion
Golgi Tendon Organ (GTO) – Located in the tendon of the muscle in series
Due to an UMN lesion γ MNs innervating plantar flexes are
with Extrafusal fibres
overfiring and hence Muscle spindle is already stimulated
Protects muscle from damage due to
before stretch
over-contraction or overstretching
3-25 muscle fibres per GTO When dorsiflexed passively 1a and 2 endings overfire causing
1b afferent fibres originate from GTO increased discharge of α MNs
➢ Since the GTO is in series with muscle fibres it is stimulated by both Hence the muscle contracts with much strength than it needs
to causing relaxation of Muscle Spindle for a short time
active contraction and passive stretch
➢ Activation of GTO causes relaxation of the muscle
Since the stretch is maintained continuously, after a short
time muscle spindle is again stimulated
When muscle is in over contraction (or overstretch)
This cycle repeats causing occurrence of a regular, repetitive,
GTO is stimulated rhythmic contraction back and forth
2) Clasp Knife Effect

Impulses generated in 1b afferent nerve endings transmitted to the spinal cord
• Since there is increased γ MN discharge, muscles are hypertonic and so
moderate stretch causes muscle contraction while strong stretch causes
1b fibres synapse with an inhibitory interneuron which synapses with α MNs of the
muscle relaxation
same muscle
Passive flexion of Elbow is attempted

Hence stimulation of GTO causes inhibition of α MNs causing relaxation of the
muscle
Triceps muscle is stretched
Motor Neuron Lesions
1. Upper MN lesions Immediate resistance is seen due to stretch reflex in the Triceps
When elbow is further flexed, Triceps is felt to be overstretched and GTO is

➢ γ MN discharge is regulated (Usually reduced) by the cortical fibres from
activated
higher centers
➢ When this inhibition is not there (eg- Spinal cord damage), γ MNs over-fire
causing hypertonic contractions in the muscles Impulses generated in 2b fibres
➢ Eg-
1) Clonus α MNs to Triceps are inhibited causing sudden loss of resistance to elbow flexion
due to Inverse Stretch Reflex
further flexion of elbow results in stretch of the relaxed Triceps
Above cycle of immediate resistance (Due to Stretch reflex)

And loss of resistance (Due to Inverse Stretch reflex) occurs repeatedly
Gives rise to a resembling movement of closing a pocket knife hence called as

Clasp-knife effect
2. Lower MN lesions
➢ It is produced by damage to cell bodies in anterior gray column or its axon

in the anterior root or spinal nerve
UMN Lesions LMN Lesions

1. Paralysis of muscles with little 1. Flaccid paralysis with muscle
of no atrophy atrophy
2. Babinski Sign 2. Loss of muscle reflexes
3. Absence of superficial 3. Muscle fasciculation
abdominal reflexes 4. Muscle contracture
4. Absence of cremasteric reflex
5. Muscle Hypertonicity
6. Exaggerated deep muscle
reflexes
7. Clonus
8. Clasp-knife Effect
Spinal cord and tracts Nucleus Position Afferents

a). Substantia Full length of the cord •Pain
Spinal cord shapes gelatinosa •Apex of the •Temperature
posterior gray •Touch
a) Central – oval column •Descending fibers from
b) Thoracic – round [Golgi type neurons] the supraspinal levels
c) Lumbar – round to oval b). Nucleus proprius •Full length of the •Senses of position and
d) Sacral – round cord movements
•Anterior to the (proprioception)
Has 2 components
substantia geletinosa •Two-point
- Grey matter discrimination.
- White matter •Vibration
c). Nucleus dorsalis •c8 to L3/L4 •Proprioceptive endings
Grey matter (Clarkes column) •Base of the (Neuromuscular spindles
posterior gray horn and tendon spindles)
1.Anterior horn/ gray column – motor
• α efferent – Innervate skeletal muscles d). Visceral afferent •T1 to L3 •Visceral afferent
nucleus • Lateral to nucleus information
• ϒ efferent – Innervate the intrafusal muscle fibers of neuromuscular
dorsalis
spindles
2.Posterior horn/gray column – sensory
• 4 nerve cell groups

• 2 groups throughout the length of the cord
• 2 groups restricted to thoracic and lumbar segments
3.Lateral gray horn Ascending Tracts (1) Lateral spinothalamic tract
• Thoracic and upper Lumbar segments only

Pain and temperature sensation received by free nerve endings
• Preganglionic sympathetic fibers
(Peripheral process of 1st order neuron)
• From anterior gray horn
• 3 nerve cell groups
Cell body in the dorsal root ganglion
Nerve cell group Position Efferent
a). Medial group •Present in most •Skeletal muscles of neck Central process enters the posterior grey horn
segments and trunk including
intercostal and abdominal Synapse with 2nd order neuron in substantia geletinosa
musculature
b). Central group •Some vertical and •Phrenic nerve (C3-C5) ->
lumbosacral segments Diaphragm Decussate obliquely anterior to central canal within one spinal
•Accessory nucleus segment (Pain fibers anterior to temperature fibers and sacral fibers
(Upper 5/6 cervical) are lateral to cervical fibers)
Sternocleidomastoid and Forms lateral spinothalamic tract and ascends upwards

trapezius
•Lumbosacral nucleus (L2 Forms spinal lemniscus of medulla oblongata
-> S1)
Unknown distribution Spinal lemniscus of Medulla Oblongata

C). Lateral group •Cervical and •Skeletal muscles of limbs
lumbosacral segments Spinal lemniscus of pons
White matter
Spinal lemniscus of midbrain
• Consists of tracts Ascending
Descending
Synapse with 3rd order neuron in ventro-postero-lateral nucleus of thalamus
Posterior limb of internal capsule
Corona radiata
Sensory cortex of postcentral gyrus

(2) Anterior Spinothalamic tract (3) Dorsal column/Medial leminiscal pathway

Discriminative touch, vibration, conscious proprioception,
Light (Crude) touch, pressure sensation received by the free nerve stereognosis and graphesthesia sensed by Meisner’s corpuscles.
endings. (Peripheral process of 1st order neuron) Pacinian corpuscles, muscle spindle and Golgi tendon organ
Cell body in the dorsal root ganglion

Cell body in dorsal root ganglion
Central process enters the posterior grey horn
Central process enters the posterior white column of same
Synapse with 2nd order neuron in substantia

Forms the dorsal column/Medial leminiscal system (Fasciculus
gracilis-fibers below T6 and fasciculus cuneatus-fibers above T6)
Decussate obliquely anterior to central canal within 2-3 spinal segments
Travels upwards through posterior white column ipsilaterally
Forms the anterior spinothalamic tract and ascends upwards
Synapse with the 2nd order neurons in the nucleus gracilis and
Forms the spinal leminiscus of medulla oblongata nucleus cuneatus at lower medulla oblongata
Spinal lemniscus of pons Great sensory decussation of axons of 2nd order neurons (Internal
arcuate fibers) at upper medulla oblongata and forms medial
Spinal lemniscus of midbrain leminiscus
Medial leminiscus at pons

Synapse with 3rd order neuron in the venerto-postero-lateralnucleus of
thalamus
Medial leminiscus at midbrain
Posterior limb of internal capsule Synapse with 3rd order neuron in ventero-postero-lateral nucleu of
Thalamus
Corona radiata Posterior limb of internal capsule
Corona radiata
(4) Posterior spinocerebellar tract (5) Anterior spinocerebellar tract
Unconscious proprioception sensed by muscle spindle, Golgi Unconscious proprioception received by muscle spindles, golgi
tendon organ, joint receptors of the trunk and lower limb tendon organ, joint receptors of trunk, upper limb, lower limb
Cell body in dorsal root ganglion Cell body in dorsal root ganglion
Central process enters the posterior grey horn Central process enters the posterior grey horn
Synapses with the 2nd order neurons in the nucleus dorsalis (Clarks column) Synapses with the 2nd order neuron in Nucleus Dorsalis (Clarkes column)
Enters the posterolateral aspect of white column on the same side

Majority of fibers cross Minority of fibers ascend
to the opposite side on the same side
Forms the posterior spinocerebellar tract
Forms contralateral anterior Forms ipsilateral anterior

Enters the medulla oblongata spinocerebellar tract spinocerebellar tract
Inferior cerebellar peduncle Through medulla oblongata, Through medulla oblongata,

pons to midbrain pons to midbrain
Ipsilateral cerebellar cortex (Doesn’t reach the cerebral cortex)

Superior cerebellar Superior cerebellar
peduncle peduncle
Contralateral cerebellar Ipsilateral cerebellar

hemisphere hemisphere
Descending Tracts (1) Pyramidal Tracts/Corticospinal tracts Spinal cord injuries
Axons of pyramidal cells situated in the cerebral cortex Spinal shock syndrome
(1/3) from the primary motor cortext, (1/3) from the secondary motor cortex, Occurs when there is acute sever damage to the spinal cord.
(1/3) from parietal lobe If there is complete section above C3 level it is fatal.
Thus 2/3 from precentral gyrus and 1/3 from post central gyrus ●Reason- Phrenic nerve (C3-C5) supplying the diaphragm is damages
impairing inspiration.
Corona radiata Below C3 -> spinal shock
3 stages
Posterior limb of internal capsule
a) Stage of spinal shock -> stage 1
Middle 3/5 of the basis pedunculi of midbrain b) Stage of reflex recovery -> stage 2
c) Stage of reflex failure -> stage 3
Broken into bundles by transverse
pontocerebellar tracts in pons a) Stage 1
All the spinal cord function below the level of the lesion are lost
Form pyramids in upper medulla oblongata
The changes occurring are given below
Lower medulla oblongata
[Mnemonic -> VASoMoToR]
80% decussate 20% no decussation
Forms and descends 1. Vasomotor changes

Forms and descends
as the lateral as the anterior
corticospinal tract corticospinal tract
(Contralateral side) (ipsilateral side) •If the lesion is above T1
Decreased sympathetic effects on heart as sympathetic

At segmental level not At segmental level
preganglionic neurons are from T1-L3 or L4
crossed crossed to the opposite
side
Decreased sympathetic effects on heart [T2-@4]
Synapse with lower motor neurons

Decreased HR Bladder, voiding reflexes recover – automatic bladder.
No inhibition or facilitation from higher centers.

•Skeletal pump is impaired Decreased COP
Hypotension
Mass reflex get activated: Pinchin/Stroking superomedial aspect of the thigh
Decreased venous return [BP=COP x PR] [COP=SV x HR]
Pudendal nerve -> S2, S3, S4 spinal segments
Decreased VEDV Decreased BP
Pelvic splanchnic nerves Rest of ANS
Profuse sweating
Reduced SV Detrusor muscle contraction
2. Autonomic changes Loss of sympathetic tone. Voiding

3. Sensory loss All sensations below the level of lesion are lost;
-Touch -Pressure -Pain -Temperature
c) Stage 3
4. Motor loss Flaccid paralysis
Typical UMN signs appear below the site of lesion
Paraplegia or quadriplegic depending on the level of the lesion.
Motor paresis or paralysis
5. Tropic changes => Muscle wasting
Hypertonia, clonus
6. Reflex loss => All spinal reflexes below the level of lesion
Hyperactive reflexes
Ex: Micturition, Defecation
Loss of superficial reflexes
b) Stage 2
Babinski sign
- Stage of shock diminishes after 2-3 weeks
No atrophy of muscles unless disuse atrophy
- Time depends on the severity of the damage
Spastic neurogenic bladder or autonomous bladder. Capacity is reduced and
- Then the spinal reflexes reappear. hyperactive.
Recovery of reflex excitability: - Due to development of denervation Reflexes which appeared in the 2nd stage may be again lost due to toxemia
hypersensitivity to mediators released by remaining spinal excitatory
•This is a stress situation Increased
endings Protein catabolism increased
circulating cortisol
Or
Sprouting of collaterals from existing neurons and motor neurons Reflex loss High concentration of urea become Increased
Flexor and adductor muscle reflexes recover first. toxic to neurons production of
urea
- Voiding reflex can be initiated on purpose by pinching/ stroking

supero-medial aspect of thigh- mass reflex.
Bladder after spinal cord transection - The voiding reflex get hyperactive
• Bladder during spinal shock period - Bladder capacity reduced (Shrunken) Spastic neurogenic
- Detrusor muscle hypertrophied bladder
Injury Causes Affected Consequences

sites
1. Complete 1.Fracture Anterior and Bilateral LMNL at
cord dislocation of lateral the level of the
transection vertebral corticospinal lesion
syndrome column tracts on Bilateral UMNL
2.Bullet or stab both sides below the level of
wound the lesion
3.Expanding
tumor
Dorsal Bilateral loss of
All bladder reflexes are lost. column of discriminative
both sides touch, vibration,
Become flaccid and unresponsive/ Atonic bladder conscious
proprioception
Sphincter vesicae contracted (Loss of inhibition from higher centers) ∴ below/at the level
Bladder becomes greatly distended, become overfilled and proper voiding is of the lesion.
impaired -> Overflow with retention. Lateral Bilateral loss of
spinothalami light touch and
Also, urine dribbles through the sphincters -> Overflow incontinence. c tracts of pressure below the
Bladder during reflex recovery period both sides level of the lesion
Anterior Bilateral loss of
Also, urine dribbles through the sphincters -> Overflow incontinence. spinothalami light touch and
c tracts on pressure below the
Bladder during reflex recovery period both sides level of the lesion
Descending Bladder and bowel
- Voiding reflex returns
autonomic function no longer
- But there is no voluntary control -> No facilitation or inhibition from fibers under voluntary
higher centers. control
∴Bladder fills and empties reflexively -> Autonomic reflex
bladder (Like infants)
Central cord Hyperextension Anterior and Bilateral LMNL at c tract on [2-3 segments
syndrome of cervical spine lateral the level of the one side below the level of
corticospinal lesion lesion]
Compression of tracts on Bilateral UMNL Posterior Ipsilateral loss of all
spinal cord both sides below the level of root of sensations at the
lesion (sacral spinal cord level of lesion
sparing)0 on one side Ipsilateral band of
Lateral Bilateral loss of pain cutaneious
spinothalami and temperature anaesthesia at the
c tracts on below the level of level of lesion.
both sides the lesion (Sacral Anterior Fracture Anterior and Bilateral LMNL at
sparing) cord dislocation of lateral the level of lesion
Anterior Bilateral loss of syndrome vertebral corticospinal Bilateral UMNL
spinothalami light touch and column tracts on below the level of
c tract on pressure below the Bullet or stab both sides lesion
both sides level of the lesion wound
(sacral sparing) Injury to
Brown- Fracture Anterior and Ipsilateral LMNL at anterior spinal
Sequard dislocation of lateral the level of the artery
syndrome/ vertebral corticospinal lesion Herniated
Hemi section column tracts on one Ipsilateral UMNL intervertebral
Bullet or stab side below the level of disc
wound the lesion Lateral Bilateral loss of pain
Expanding spinothalami and temperature
tumor c tracts on below the level of
Dorsal Ipsilateral loss of both sides lesion
column on discriminative Anterior Bilateral loss of
one side touch, vibration and spinothalami light touch and
conscious c tracts on pressure below the
proprioception both sides lesion
below the level of •Dorsal
lesion column
Lateral Contralateral loss of intact
spinothalami pain and Syringomyeli Developmental Anterior and Dissociated
c tract on temperature [1 or 2 a abnormality in lateral sensory loss with
one side segments below the formation of spinothalami loss of pain and
level of the lesion] central canal c tracts temperature while
Anterior Contralateral loss of Cavitation and *Dorsal touch is spared as
spinothalami light touch and gliosis of the columns dorsal columns are
pressure central region intact intact.
Anterior Paralysis and Multiple Demyelination Ascending Multiple

horn cells atrophy of muscles sclerosis of ascending and neurological
[Small muscles of and descending descending symptoms
hand] tracts tracts Optic neuropathy
Pyramidal Lower extremity Spastic paraparesis
tracts spastic paraparesis. Vertigo, deafness
Dysarthria,
dysphagia ->
Loss of upper limb brainstem
reflexes demyelination
Tropic changes Pernicious Vitamin B12 Myelination
Skin ulcers anemia deficiency get affected
Scars Posterior/
Nail lateral white
dystrophy columns
Of syrinx extend to Peripheral
brainstem -> nerve
Syringobulbia degeneratio
Tongue n
atrophy Tabes Late Dorsal Unable to recognize
Fasciculatio Dorsalis manifestation of columns limb position and
ns syphilis joint position
Bulbar palsy Astereognosis
Nystagmus Loss of two-point
Horners discrimination
syndrome Loss of
Hearing loss graphesthesia
Poliomyelitis Acute viral Lower motor LMN paralysis of Loss of vibratory
infection of neurons muscles supplied by sense
neurons of the the involves LMN Positive rhombergs
anterior gray Wasting and sign
column and paralysis of muscles Sensory ataxia ->
motor nucleus Paralysis can broad base high
of cranial nerves extend to stepping gait ->
intercostals and stamping gait
diaphragm leading Loss of tendon
to respiratory reflexes
failure. Unsteadiness of
*No sensation loss finger nose test
Posterior Irregular sharp Duplicity Theory

roots momentary
[Specially in stabbing pain
lower (Lighting pains) • Rod Cells are specialized for Scotopic vision (i.e. night vision):
thoracic involving calf, thigh o It has a low visual threshold (i.e. the minimum light intensity at
lumbosacral or ankle. which an action potential is generated in the ganglion cells)
regions]
o It has a low visual acuity, since each rod cell synapses with
several bipolar neurons.
o It has a low colour differentiation ability, since the visual
Vision pigment (rhodopsin) shows low specificity to colour.
• Cone Cells are specialized for Photopic vision (i.e. colour vision):
o It has a high visual threshold (i.e. light of a higher intensity is
Retina
needed for phototransduction)
o It has a high visual acuity, since each cone cell synapses with a
• Innermost lining of the eye, & consists of several types of cells arranged single bipolar neuron (one-to-one connection)’.
in layers: o It has high colour differentiation ability, since there are 3
o Rods & Cones (Photoreceptor cells) – outermost layer, adjacent specific types of cone cells with pigments specific to red, green
to the Choroid layer or blue (Young-Helmholtz theory).
o Bipolar Neurons (1st order neurons) – middle layer, which also • So, rod cells are needed to see in dim light & to detect the absolute
has Horizontal cells & Amacrine Cells level of light, while cone cells are used to detect changes in intensity
o Ganglion Cells (2nd order neurons) – innermost layer; axons of of light, colour vision & visual acuity.
these cells are found in the Optic Nerve
NOTE: At the threshold light intensity at which cone cells are just
• rd
3 order neuron cell bodies of the visual pathway are in the Lateral
stimulated, rod cells are maximally stimulated.
Geniculate Body of the Thalamus
• Rods & cones synapse with bipolar neurons, which in turn synapse
with ganglion cells.
• In addition, the retina has Muller cells (glial cells).
• Horizontal cells connect photoreceptors, Amacrine cells connect
ganglion cells & bipolar neurons.
• Optic Disc – position of the optic nerve entering the eye; No
photoreceptors present, known as the blind spot
• Macula – avascular region near the posterior pole. Contains the Fovea
Centralis, which is devoid of Rod cells & has the greatest visual acuity;
ideally an image is focused onto this part.
• In the extrafoveal parts of the retina, Rods are more numerous
Visual Acuity Ionic Basis of the Photoreceptor Mechanism (Phototransduction)
• Defined as the shortest distance by which 2 lines can be separated & Conformational change in
Light causes
still be seen as 2 lines. Rhodopsin; Opsin
degradation of
• Measured clinically using Snellen Charts; patient is placed 6m (20ft) activates Transducin; a G-
Retinal in Rhodopsin
away from the chart, one eye being closed, the patient is asked to read Protein
letters of decreasing size. The last line the patient can read is noted &
the visual acuity is reported as:
𝑉𝑖𝑠𝑢𝑎𝑙 𝐴𝑐𝑢𝑖𝑡𝑦 (𝑉𝐴)
Transducin activates
𝐷𝑖𝑠𝑡𝑎𝑛𝑐𝑒 𝑎𝑡 𝑤ℎ𝑖𝑐ℎ 𝑡ℎ𝑒 𝑝𝑎𝑡𝑖𝑒𝑛𝑡 𝑠𝑒𝑒𝑠 (𝑖. 𝑒. 6𝑚)
= cGMP Decreased Phosphodiesterase
𝐷𝑖𝑠𝑡𝑎𝑛𝑐𝑒 𝑎𝑡 𝑤ℎ𝑖𝑐ℎ 𝑎 𝑛𝑜𝑟𝑚𝑎𝑙 𝑝𝑒𝑟𝑠𝑜𝑛 𝑐𝑎𝑛 𝑠𝑒𝑒 𝑡ℎ𝑒 𝑙𝑎𝑠𝑡 𝑙𝑖𝑛𝑒 𝑡ℎ𝑒 𝑝𝑎𝑡𝑖𝑒𝑛𝑡 𝑟𝑒𝑎𝑑𝑠
• A VA of 6/6 is normal, 6/36 means an impaired visual acuity, & 6/5 is

supernormal VA (need not be treated) Closes Na+ channels Rod Cell Hyperpolarized
• If the patient can’t read the 1st line at 6m, he is moved 1m closer & so
on until he can read the 1st line; e.g. VA= 5/6 means very poor VA.
• VA is affected by:
o Optical Factors – State of image forming mechanisms Decreased Glutamate release by rod cell
o Retinal Factors – State of cones
o Stimulus Factors – e.g. Brightness, contrast, length of stimulus
Depolarizing signal via
• Age-related Macular degeneration (AMD) is a disorder in which central
Bipolar Cell causes Action
visual acuity declines with age.
Potential generation in
Photoreceptor Mechanism Ganglion cell
• Receptor (Generator) potentials of rods & cones are localized, graded
potentials whose amplitude depends on light intensity.
• Receptor potentials in rods/cones result in development of action
potentials in ganglion cells. • The above occurs in the presence of light. When dark, Na+ channels in
• Rods, cones & horizontal cells are hyperpolarizing, while bipolar cells segments of rods & cones are open; there is a constant release of
are either hyperpolarizing or depolarizing to Ganglion cells. Glutamate.
• Phototransduction in cones occurs via a similar process.
• Melanopsin is a photopigment in ganglion cells which is involved in the
circadian rhythm (independent of rod & cone cells)
Principles of Optics Refractive Errors (Defects in Vision)
• Refraction of light focuses an image on the retina. The cornea is a 1. Hyperopia/Hypermetropia – Far Sightedness
mono-convex lens; the lens of the eye is a biconvex lens. Air,
aqueous humor & vitreous humor act as refractive media.
• Eyeball is shorter than normal, so light from a near object (diverging
• Principle Focus: Point to which refracted light rays converge (ideally
light rays) are focused behind the retina. Distant objects (parallel light
onto the macula of the retina). The principle focal distance is the
rays) can be focused & seen clearly.
distance between the lens & the principle focus.
• Sustained accommodation can partially compensate but leads to
• An object more than 6m is taken as being at an infinite distance
headaches & strabismus.
since light rays from it are more or less parallel (basis for distance
taken in VA test). An object closer than 6m produces divergent light • Correction: Glasses with convex lenses, which converge the light rays
rays. onto the retina.
1
• 𝐷𝑖𝑜𝑝𝑡𝑒𝑟 = 𝑃𝑟𝑖𝑛𝑐𝑖𝑝𝑙𝑒 𝐹𝑜𝑐𝑎𝑙 𝐷𝑖𝑠𝑡𝑎𝑛𝑐𝑒 (𝑚)
• At rest the human eye has a refractive power of 60D (dioptres)
• The retinal image is inverted & formed on the opposite side of the
visual field (e.g. an object in the nasal visual field stimulates the
temporal part of the retina)
2. Myopia – Near Sightedness 3. Astigmatism

• Curvature of the cornea is not uniform. Light rays striking the abnormal
region refracts to a different focus, so part of the retinal image is
• Antero-posterior diameter of the eye is too long, so light from a distant
blurred.
object (parallel rays) is focused in front of the retina. Closer object may
• Correction: Cylindrical lens.
be focused & seen clearly.
• Correction: Glasses with concave lenses, which diverge the light rays
such that they are focused onto the retina.
4. Presbyopia (hathalis adiriya)
• Progressive hardening of the lens with age leads to a decrease in the
ability to accommodate (lens thickening). Becomes significant at 40-45
years.
• Near point of vision recedes, but visual acuity is normal.
• Correction: Biconvex lens
5. Strabismus – Misalignment of eyes

• If one eye is turned inwards, it is termed internal strabismus or
Esotropia. If it is turned outwards, it is termed external strabismus or
Exotropia.
• Images don’t fall on the corresponding point of the retina, leading to
diplopia.
• I the condition is chronic one retina is suppressed by the cerebral
cortex, leading to a permanent decrease in visual acuity in one eye
(suppression scotoma).
• So it should be corrected early by forcing the weaker eye to work (i.e. by
covering the stronger eye or using atropine on the stronger eye).
6. Amblyopia (Lazy eye)
• Vision in one eye is blurred due to a refractive error. If chronic, may lead
to permanent loss of visual acuity in one eye (amblyopia ex anopsia).
This defect may coexist with strabismus.
Pupillary Light Reflex
• Sudden exposure of one eye to bright light results in constriction of the

pupil in the same eye (direct light reflex) & of the other eye
(consensual light reflex).
• Pathway:
o Impulses are transmitted through the optic nerve, optic chiasma
& optic tract.
o They bypass the Lateral Geniculate Body (LGB) of the thalamus
to relay (synapse) at the Pretectal Nucleus of the midbrain.
o From the pretectal nucleus, the impulses travel to the Edinger-
Westphal Nuclei of both oculomotor nerves.
o Impulses travel via the oculomotor nerve (parasympathetic
fibres lie peripherally), the fibres relay in the Ciliary ganglion &
pass via the short ciliary nerves to the Sphincter pupillae
muscle, which on contraction causes pupillary constriction
(miosis).
Accommodation/Near Reflex • Pathway:

o Optic nerve, chiasma & tract
o Lateral Geniculate Body of the Thalamus
• At rest, the eye lens is held elongated & under tension by suspensory o Primary Visual Cortex via Optic radiation
ligaments (Zonules). The sphincteric Ciliary muscles are relaxed. o Frontal Eye field
o Main Oculomotor nucleus & Edinger-Westphal nucleus
o Effectors (Parasympathetic fibres relay in the ciliary ganglion)
Accommodation
• As a distant object is brought nearer, the Ciliary muscle contracts. The Argyll-Robertson Pupil
sphincter –like action of its circular fibres bring the ciliary body closer,
thus relaxing the suspensory ligament & thickening & shortening the • Occurs due to a neuro-syphilitic lesion of the pretectal fibres to the
eye lens. Edinger-Westphal nuclei.
• This increases the refractive power of the lens by increasing the • Results in the loss of the direct & consensual light reflexes (usually
curvature (Up to 12D is added to the resting power). bilaterally) while the Accommodation reflex is intact.
• This is because the accommodation reflex pathway passes through the
lateral geniculate body & not the pretectal nucleus.
Near Response
• It is a 3-part reflex in response to bringing an object close to the eye:

o Accommodation (Explained above)
o Pupilar constriction
o Contraction of the Medial Rectus Muscle – eyes move medially
• The first 2 are controlled by the parasympathetic Edinger-Westphal
Nucleus, while the 3rd is by the motor nucleus; all 3 being transmitted
via the oculomotor nerve.
• NOTE: Practically, near response & accommodation are considered the
same.
Visual Pathway • Visual field of the eye: The total area in which objects can be seen in
the peripheral vision as the eye is focused onto a central point.
• The total visual field is divided into 4 quadrants:
• Images in in each visual field fall on the opposite part of the retina, &
visual information is conveyed in the corresponding retinal fibres of the
optic nerve E.g. Images in the upper temporal visual field fall on the
lower nasal part of the retina.
• Nasal retinal fibres of the optic nerve of each eye carry the temporal
visual field of the same eye. Similarly, the temporal retinal fibres carry
the nasal visual field. The Macula also gives rise to nasal & temporal
fibres.
• The nasal retinal fibres (carrying the temporal visual field info) cross to
the opposite side at the optic chiasma. Temporal retinal fibres remain
uncrossed.
• Thus, each optic tract contains fibres carrying visual information from
the opposite visual field.
• E.g. The Left optic tract contains:
Left temporal retinal fibres (nasal visual field of the left eye)
o Right nasal retinal fibres, which cross (temporal visual field of Lesions of the Visual Pathway
right eye).
o Left nasal visual field + right temporal visual field = Right Visual
Field (with respect to both eyes)
• Fibres from the upper retinal quadrants (lower visual field) synapse at
the medial part of the Lateral Geniculate Body of the thalamus & vice
versa.
• Primary Visual Cortex: Located in the Occipital pole of the brain,
around the Calcarine sulcus:
o The Left Visual Field is represented in the Right visual cortex
o The Inferior Visual Field is represented in the superior lip of
the calcarine sulcus (i.e. above the sulcus)
o Visual info from the Macula travels to the posterior 1/3
(occipital pole) of the visual cortex, which has a dual blood
supply from the PCA & MCA (it has a large representation as it is
the region with the highest visual acuity). Macular vision is also
divided as above.
o Peripheral vision (i.e. visual field excluding the macula) is
represented radially around the occipital pole
o Function of the primary visual cortex is to differentiate
information about colour from movement & to combine the
input of both eyes. It converts vision into short line segments.
1. Circumferential Blindness – Hysteria or Optic Neuritis (due to infection) 7. Scotoma – The loss of a small patch of vision (a blind spot) in an
2. Total Blindness of one eye – Complete section of one optic nerve otherwise normal visual field. E.g. A left side central scotoma occurs if
(blindness in same side eye). the right-side occipital pole (macular region) is damaged.
3. Nasal Hemianopia – Partial lesion of the optic chiasma on its lateral side
[NOTE: Complete/partial blindness can occur with intact pupillary light
(i.e. temporal retinal fibres) would cause a loss of the nasal visual field
reflexes if the lesion is beyond the optic tract]
on the same side
4. Bitemporal Hemianopia – Sagittal section of the optic chiasma most
commonly due to a pituitary tumour (lies directly under the chiasma).
This damages the nasal retinal fibres (carrying the temporal visual Colour Vision
fields) as they cross at the chiasma.
5. Contralateral Homonymous Hemianopia –
• Colour vision has 3 attributes: Hue, Intensity & Saturation.
o Hemianopia – Half of the visual field is lost.
• The phototransduction process for colour vision is similar to that of rods
o Homonymous – Visual field loss is of the same side in both
(see above).
eyes
• Young-Helmholtz theory states that in humans, there are 3 kinds of
o Contralateral – Visual field loss is of the opposite side to that
cone cells, each having a different photopigment that is maximally
of the lesion
sensitive to one of the 3 primary colours (Red, Green, Blue).
o Occurs due to a lesion of:
• Genes for Rhodopsin is on chromosome 3, for the blue pigment on
i. Optic Tract (No Macular Sparing)
chromosome 7 (i.e. both are separate), while the genes for red & green
ii. Optic Radiation (Macular Sparing)
opsins are both on the ‘q’ arm of the X chromosome (red & green
iii. Visual Cortex (Macular Sparing)
opsins also have an almost identical amino acid sequence).
o Macular vision is not spared in a lesion of the optic tract as the
fibres are tightly packed, & all are usually damaged. Colour Blindness
o In the optic radiation, since the fibres are loosely packed,
macular fibres may be spared.
o In the visual cortex, the macular region is separate, large & has • Colour blindness is the inability to see one or more colours.
a collateral blood supply (described above), so macular visual • Normally, humans are trichromats, i.e. they can see all 3 primary
field is usually spared. colours (RGB) & their complementary colours.
o E.g. Lesion of the left visual cortex results in the loss of the right • Dichromats have 2 functioning cone systems, while Monochromats
visual field (I.e. temporal visual field of the right eye & nasal have only 1.
visual field of the left eye), with the central (macular) region of • The most common form of colour blindness is Red Green Colour
the affected side being intact. Blindness, which occurs due to a mutation in the ‘q’ arm of the X
6. Contralateral Quadrantanopia – A single quadrant of the visual field is chromosome & thus show X-Linked Recessive inheritance. These
affected, usually in both eyes. E.g. A lesion of the superior lip of the individuals may be dichromats or trichromats with a cone anomaly.
calcarine sulcus on the left side results in the loss of the lower nasal VF They see their version of red or green but have difficulty differentiating
of the left eye & lower temporal VF of the right eye. shades of those colours.
• Achromatopsia – A form of colour blindness that occurs due to the o A more gradual but larger decline in visual threshold due to Rod
damage to the V8 area of the primary visual cortex. adaptation (no significant decline in visual acuity)
• Cyanopsia – Vision is shaded with a blue-green filter like effect. May be
Light Adaptation is simply the disappearance of the dark adaptation, as
a side effect of taking Phosphodiesterase inhibitors for erectile
photopigments are rapidly degraded when moving from a dim light to a
dysfunction (e.g. Sildenafil) since they inhibit the both the Retinal &
bright light. It takes 5 minutes (pigment degradation is faster than
penile form of the enzyme.
synthesis).
• Colour blindness is tested clinically using Ishihara charts.
Use of Red Goggles to minimize time duration of dark adaptation
Dark Adaptation • Pilots use red goggles in the air as entry into clouds suddenly decreases
the light intensity, which causes a rapid impairment of vision which is
• It is defined as the decline in visual threshold of the photoreceptor dangerous
cells as a person moves from a well-lit area to a dimly lit environment • Red goggles allow only red light & blocks all other wavelengths. Thus,
(sometimes pupilar dilatation is also included). degradation of rhodopsin stores in rods is minimized while sufficient
• Visual Threshold – The minimum light intensity at which light is vision is maintained by the cone system responsible for red light in the
detected by rods or cones. well-lit environment.
• So, the rhodopsin store is available once they enter dim light,
decreasing the time of adaptation from 20 mins to almost instantly.
• In a well-lit environment, due to the constant bombardment of light
rays, Photopigment stores of the rod & cone cells are depleted.
Therefore, a high light intensity is needed to detect light in this state Eye Movements
(I.e. the visual threshold is high).
• When this person moves to a dimly lit environment, it takes some time
• There are 4 main types of eye movements:
for the photopigment stores (e.g. rhodopsin) to replenish. This delay is
1. Saccades – Gaze shift between stationary objects. Controlled by
called the dark adaptation period & takes about 20 minutes for a near
the frontal eye field & superior colliculus
maximum adaptation.
2. Smooth Pursuit Movements – Controlled by the cerebellum
• Once the visual pigment stores are built up, even a low intensity light
3. Vestibular Movements – Adjustments of eyes in response to
source will cause the degradation of many pigment molecules, creating
linear/ rotational head movements (vestibulo-ocular reflex vie
generator/ receptor potentials high enough to detect light (i.e. an action
the vestibular nuclei, medial longitudinal fasciculus & motor
potential is generated in the ganglion cell).
nuclei of the Cranial nerves III, IV & VI.
• This adaptation occurs in 2 stages:
4. Convergence Movements
o A sharp but short decline in visual threshold due to cone
• All of the above require an intact visual cortex
adaptation (occurs first). Since cones are responsible for visual
acuity, there is a sharp decline in visual acuity initially. [NOTE: Also refer the CN III, IV, VI & the extraocular muscle movements.
* Depolarization cause hair cells to release a neurotransmitter-

Physiology of Hearing glutamate(probably) - it initiates depolarization of afferent neurons
External ear semicircular canals
Middle ear hearing utricle equilibrium Cochlea
Cochlea saccule
Inner Ear(labyrinth)
Made of 2 parts one within another
1.Bony labyrinth - filled with perilymph low [K+]
2.Membranous labyrinth - filled with endolymph high [K+]
Receptors
• are hair cells
• Hair cells in
semicircular canals detect - rotational acceleration
utricle detects - linear acceleration in horizontal direction
saccule detects - linear acceleration in vertical direction
cochlea detects - sound waves
Electrical response
Sound Transmission
sound waves organ of corti action potentials in auditory nerve
Sound waves
Enter through external auditory meatus
shorter stereocilia are pushed towards taller ones Travels in the auditory canal and vibrates the tympanic membrane
tip links stretch and opens ion channels in its taller neighbor vibrations imparted to manubrium of malleus
Ca2+ , K+ enter via cation channels and produce depolarization vibrations trasmitted to incus
myosin based motor in the taller stereocilium moves the channel towards the base movements of footplate of stapes
tension in the tip link is released and reach resting membrane potential (-60mV) series of travelling waves in perilymph of scala vestibuli
vibrations over Reissner membrane and then in scala media ➢ posteromedial part- reception of sounds with
high frequency
basilar membrane is depressed into scala tympani
secondary auditory cortex- recognition and interpretation
of sound waves
Hairs of inner hair cells (primary sensory receptors) are bent by displacement of fluid in
fluid between tectorial membrane and underlying hair cell scala tympani • Auditory areas have marked hemispheric specialization
Hairs of outer hair cells - embedded in tectorial membrane - • Eg. Wernicke area - During language processing it's more active on
respond the same way waves dissipated into air left side
at round window Right side - concerned with melody, pitch and sound intensity
Central pathway
Generation of action potential in peripheral fibres of cochlear nerve
impulses reach spiral ganglion of the cochlea
central process enters brainstem at lower border of pons with vestibular nerve
At cerebellopontine angle.
lateral to facial nerve
fibers divide to synapse with anterior and posterior cochlear nuclei on the
surface of inferior cerebellar peduncle
second order neurons synapse with posterior nucleus of the trapezoid body and
superior olivary nucleus of same or opposite side
Axons ascend through posterior part of pons and midbrain - form a tract called
lateral lemniscus (contains 3rd order neurons of both sides)
on reaching mid brain, fibers
terminate in nucleus relay in medial

of inferior colliculus geniculate body of thalamus some relay in small
groups of nerve cells
* center for auditory acoustic radiation of internal capsule collectively called
reflexes nucleus of lateral
primary auditory cortex (areas 41and 42) lemniscus
➢ anterolateral part - reception of lower tones

Tympanic Reflex Conduction of Sound
• Reflex contraction of tensor tympani & stapedius muscles. ▪ Ossicular conduction- conduction of sound waves to fluid of inner ear via
• Tensor tympani- Pulls manubrium of malleus inwards tympanic membrane, auditory ossicles. (main pathway of hearing)
• Stapedius- Pulls footplate of incus outwards ▪ Air conduction - sound waves initiate vibrations of the secondary tympanic
• It's a protective reflex membrane which closes round window (unimportant in hearing)
• Prevents strong sound waves causing excessive stimulation of auditory ▪ Bone conduction - vibrations of bones of the skull fluid in inner ear
receptors Generation of AP in 1s t order neurons
• It doesn't protect from brief intense stimulations as gun shots since the
Deafness
reaction time is 40-160ms
1) Conductive deafness
Sound localization • Impaired sound transmission in the external or middle ear

• Determination of the direction from which a sound originates in the • Impact all sound frequencies
horizontal plane • Causes - Plugging of external auditory canal with wax or foreign bodies,
It depends on, otitis externa, otitis media, perforation of the ear drum, osteosclerosis
• detecting the difference in time between the arrival of the stimulus in 2
ears If cochlea and nerve are still intact but the tympanium ossicular system is destroyed
• and the difference in phase of the sound waves on 2 sides - sound waves can still be conducted to cochlea by bone conduction.
• Sound localization is disrupted by lesions in auditory cortex 2) Sensorineural deafness
• Due to impairment of the cochlea (loss of hair cells), the CN VIII or central
Identification of Sound auditory pathways.
1) Loudness - correlated with amplitude • Often impairs the ability to hear certain pitches while others are
Greater the amplitude louder the sound unaffected.
Expressed in decibel scale
Causes
2) Pitch- correlated with frequency
• Use of various chemicals(ototoxins)
Frequencies audible to humans range between 20-20 000Hz
Eg.1. Antibiotics:-Aminoglycoside antibiotics as streptomycin, gentamicin
obstruct the mechanosensitive channels in hair cells cause the cells to
3) Quality of sound- harmonic vibrations provide the sound its quality(timbre)
degenerate
• Musical sounds are made of a wave with a primary frequency 2. Loop diuretics
(determines pitch) plus harmonic vibrations
• Tumors of CN VIII and cerebellopontine angle
• Sound waves with repeating patterns- produce musical sounds
• Damage to hair cells by prolonged exposure to noise.
• Aperiodic nonrepeating vibrations- noise 3) Presbycusis
• Gradual loss of hearing with age
Masking
• Due to gradual cumulative loss of hair cells and neurons.
Presence of one sound reduces the ability to hear other sounds.
• In most cases hearing loss is a multifactorial disorder and single gene
mutations also have caused hearing loss.
Due to relative/absolute refractoriness of previously stimulated auditory receptors
and nerve fibers to other stimuli.
Tests for hearing Audiometry
• Auriscopic examination of the external ear passages and ear drums • Auditory acuity is measured by an audiometer.
by"oroscope" • The device presents pure tones of various frequencies through ear phones.
• Observe the light reflex in a normal healthy ear. • Threshold intensity is determined at each frequency and plotted on a
• Normal color of tympanic membrane - whitish graph as a percentage of normal hearing.
• It also has a mechanical vibrator for testing bone conduction from the
Important factors considered in tests for hearing mastoid process of the skull into the cochlea.
i. sound entering the ear is masked by sounds from the environment. Refer the practical book pg 64 for the tests
ii. air conduction is better than bone conduction.
Basic tests
• Ask the patient to close his eyes and the examiner whispers in one of the
patient's ears while applying finger pressure on the other ear's tragus.
• Ask the patient to repeat what was whispered.
• Repeat for the other ear.
• If there's an impairment of hearing we should assess if it's a conductive

deafness or a sensorineural deafness.
For that Weber's lateralizing test is done to identify the defective ear
and Rinne’s test is next done to both ears to confirm a conductive or a
sensorineural deafness.
1.Weber's test - Place the base of a vibrating tuning fork on the vertex and
ask the patient whether the sound comes from one ear or the other
➢ In conductive deafness- sound is heard better in the abnormal ear
• Sound is heard due to bone conduction

• Absence of masking effect.
➢ Nerve deafness- sound is heard better in the normal ear.
2.Rinne's test - Base of a vibrating tuning fork is 1st placed on the patient's mastoid
process - ask whether a sound is heard.
When the sound is no longer audible hold the tuning fork in front of the ear- ask
whether a sound is heard.
➢ conductive deafness- sound is heard when the tuning fork is placed on the
bone
but not when it's held in front of the ear.
➢ nerve deafness- no sound is heard at any point.

Balance and vestibular system Taste

Rotational acceleration
• a visceral sensation
Linear acceleration
• must dissolve in saliva
Sweet Tip of tongue Activates adenylate
Crista in semicircular canal ampulla
Horizontal Vertical cyclase cAMP, close K+
• Endolymph displaced in opposite channels
bitter Back of tongue Increase production of
Macule in Macule in direction of rotation
IP3 via G proteins
utricle saccule • Fluid pushes on copula deforming it Increase intracellular
• Bend the processes of hair cells calcium
• Otoliths move in • Depolarize salty Front half of each Activates amiloride
opposite direction (deceleration- endolymph moves in side sensitive Na+channels
• Distorting hair cells same direction of rotation) sour Posterior half of each Increase intracellular
❖ (when endolymph moves in side H+,Block Na+ channels
• Depolarize
opposite direction- inhibit umami Triggered by
• Ap generated monosodium glutamate
firing
Activation of glutamate
❖ When it moves in the same receptor
direction – start firing)
• gustatory receptor cells are found within taste buds, which are found
Fundus of internal acoustic meatus
within papillae
(posterosuperior quadrant – anterior ,lateral semicircular • papillae
canals,utricle - fungiform papillae- anterior 2/3 of tongue, has five taste buds
- circumvallate papillae- posterior part of tongue, has 100 taste buds
Posteroinferior quadrant-posterior semicircularcanal ,sacule)
- foliate papillae-lateral border of tongue, numerous taste buds
- filiform papillae-
1st order neuron cell bodies in vestibular ganglion
Central processes form vestibular nerve

• taste sensation from anterior 2/3rd of tongue –lingual ,chorda tympani
Join with cochlear nerve and pass through pontine cistern nerve, neurons in geniculate ganglion, to NTS through VPL nucleus of
thalamus to post central gyrus
Inferior cerebellar peduncle and lower pons
• sensation from posterior 1/3rd of tongue – glossopharyngeal nerve
Anteriot ,posterior,medial, lateral vestibular nuclei
• palate, pharynx, epiglottis- vagus nerve, NTS,VPL of thalamus to post

Medial Descend central gyrus
Vestibular Inferior cerebellar
area in post peduncle longitudinal uncrossed
central gyrus fasciculus (vestibulospinal)
Cerebellum CN3,4,6
• ABNORMALITIES- Ageusia-absence of sense of taste eg- captopril, penicillin

Cerebral circulation
Hypogeusia-impaired sense
Dysgeusia-disturbed sense of flavor •Arterial supply
Aorta Common carotids Internal carotid artery

Sense of smell Subclavian artery Vertebral artery Basilar artery
• Cranial nerve 1 is responsible for the olfactory sensation Circle of Willis 2 Internal carotid artery
• Odorant molecules bind with odorant receptors
Basilar artery
• Located in cilia / unmyelinated processes of bipolar olfactory neurons in
olfactory epithelium in the upper nasal cavity. •Venous drainage
• Odorant receptors are G protein coupled receptors
Deep veins Dural sinuses
1. When odorants bind, their alpha subunit
dissociate and activates adynyl cyclase enzyme Internal jugular veins
2. Increase cAMP levels
Small drainage through
3. cAMP activates Na+ ,Ca2+ cation channel and
induces a Ca2+ influx - Ophthalmic venous plexus
4. receptor neurons are depolarized - Pterygoid venous plexus
• course peripheral fibres of these receptor neurons project into the nasal - Paravertebral veins
cavity •Main features of cerebral blood flow
• central processes of the receptor neurons pass via cribriform plate into
anterior cranial fossa(1st order neurons) Even though the brain is only 2% of the body weight the cardiac output for brain is
• they relay with dentrites of mitral and trufted cells and form olfactory 15%
glomeruli in olfactory bulb Average cerebral blood flow – 54ml/100g/min
• axons of 2nd order neurons form the olfactory tract and travels towards
anterior perforated substance For the whole brain maintained at 750ml/min
• some fibres decussate and form medial olfactory striae The cerebral cortex and the cerebellum receive a large blood flow, which are active
• some fibres pass to ipsilateral all the time
primary olfactory area
The largest flow is to the inferior colliculus and to their nuclei
pre amygdaloid
prepiriform areas and connect with frontal The flow is greater in grey matter than in white matter an in axons
cortex
compared to cell bodies.
•Fluctuations in regional blood flow

orbito frontal cortex is responsible for discrimination of different smells(eg-
humans can identify more than 10 000 different odours Fluctuations in regional blood flow directly varies with activity of that region
several cortical areas are responsible for olfactory memory and amygdaloid is Mental activity doesn’t increase total blood flow
responsible for emotional changes regarding olfaction.
Eg : For a right handed person •Autoregulation
Verbal task flow to left hemisphere Similar to heart and kidneys as the brain can tolerate wide swing in BP with
little changes in blood flow
Spatial task flow to right hemisphere
The cerebral vasculature rapidly adapts to changes in cerebral perfusion
When looking at an object the blood flow to the occipital cortex is increased
pressure (CPP) (10-60s).
leading to increase in co2 and H+ which will in turn increase the local blood
flow. ↓ in CPP – Cerebral vasodilation
•Monro–Kellie doctrine ↑in CPP – Vasoconstriction
In adults the brain parenchyma, spinal cord, spinal fluid and cerebral vessels IN normal individuals MAP is maintained between 60-160 mmhg
are in a rigid bony skull
Beyond these limits, blood flow becomes pressure dependent.
Blood = 75ml
Pressure above the limit can disrupt the blood brain barrier leading to
Brain = 1400g cerebral edema and hemorrhage.
CSF = 75ml
The brain parenchyma and CSF are relatively incompressible
•Methods to measure CBF
1. Kety methods – Inhaled Nitrous oxide

C.B.F=Amount of N2O taken by the brain/Arterio venous difference
of N2O across the brain
2. Radioactive substances – Iodine, 133Xe
3. CT and fMRI
4. Single photon emission CT – “SPECT”
•Factors affecting total cerebral blood flow

1. Arterial pressure at level of brain
1. Mean arterial pressure at level of brain Eg: ↓ B.P
2. Mean venous pressure at level of brain Severe ↓ B.P - ↓↓ Cerebral blood flow
3. Intracranial pressure 2. Venous pressure Effective perfusion pressure
4. Viscosity of blood
5. Local constriction and dilation of arterioles Compresses cerebral vessels
Cerebral blood flow

3. ↑ Intracranial pressure NOTE: BBB is very immature in neonates. IN severe neonatal jaundice, bilirubin
can cross the immature BBB and get deposited in basal ganglia resulting in a
Compresses cerebral vessels condition called kernicterus. In adults bilirubin cant cross the barrier.
4. Changes in viscosity Functions
↑Viscosity of blood (polycythemia)
1. Maintain consistency of environment of the brain.
2. Protection of brain from endogenous and exogenous toxins.
↓Cerebral blood flow
3. Prevent escape of neurotransmitters into the general circulation.
5. Caliber of arterioles
- Local vasodilator metabolites Clinical significance of BBB
- Autoregulation
1. Dopamine, serotonin do not readily cross the barrier but their precursors
- Endothelial substances cross the barrier with ease.
- Circulating peptides – Angiotensin 11 L-DOPA given as treatment for Parkinson’s
- Vasomotor nerves NOTE: L-DOPA cross the barrier, then convert into Dopamine by DOPA
decarboxylase enzyme.
•Clinical importance of cerebral circulation
2. In meningitis, meninges become more permeable locally, at the site of
Most important is “stroke”/Cerebrovascular disease (SVC)/ Cerebrovascular inflammation, so permitting sufficient antibiotic to reach the infection
accident (CVA) 1. Chloramphenicol
2. Tetracycline
3. Tumors develop new blood vessels with more fenestrations. Lack
Blood brain barrier of astrocytes and tight junctions. So, the BB is very weak or
● BBB is formed by the tight junctions between capillary endothelial cells in the absent. Radioactive iodine labelled albumin cant cross the BBB,
brain and between the epithelial cells of the choroid plexus. but they can enter the tumor tissue through weak BBB and helps
in identifying the location of the tumor.
● This is a selective permeable barrier which is formed at 3rd month of fetal
gestation. Breakdown of integrity
● Passive diffusion across the barrier is limited. Carrier mediated transport and 1. Irradiation
active transport systems are more prominent. 2. Infection, injury
3. Tumor
Transport mechanisms 4. Increase in BP
5. IV fluid injection
1. Passive diffusion – H2O, CO2, O2 lipid soluble free forms of steroid
hormones Circumventricular organs
2. Facilitated diffusion – Glucose through GLUT1 (Infants with GLUT1
deficiency develops low CSF glucose leading to seizures and delayed Areas with fenestrated capillary endothelium or the areas with no BBB.
development)
1. Posterior pituitary
Thyroid hormones, Ach, Nuclei acid precursor and AA transport through
2. Area postrema
carrier mediated.
3. Organum vasculosum of the lamina terminalis
3. Protein bound molecules; proteins are impermeable.
4. Subfornical organ
When ICP is raised the pressure is transmitted alone optic nerve causing
CSF papilledema
CSF is a clear, colorless, body fluid found in the sub arachnoid space (Between
•Functions of CSF
arachnoid and pia mater) ventricles and spinal cord.
1) Cushions and protects the CNS from trauma
•Formation
2) Provides mechanical buoyancy and support the brain
Choroid plexus – 50% 3) Serves as a reservoir and assists in regulation of contents of the skull
4) Nourishes the CNS
Around blood vessels 5) Removers metabolites from CNS system.
6) Important for acid bas regulation foor control of respiration
Along ventricular walls
In air brain weighs about 1400g but in a container of CSF net weigh is of 50g
•Composition of CSF
•CSF analysis (Cytology)
Similar to brain ECF. Inorganic salts similar to blood plasma f
Increase in pressure due to
Formed as plasma ultrafiltrate and through active secretion of solutes/
- Infection (meningitis)
Volume -150ml
- Cerebral edema
Rate of production – 550ml/day - Space occupying lesion (brain tumor, abscess or hematomas)
Glucose is about half to two third of blood. Only a trace of protein Cloudy appearance (Turbidity) -> Presence of polymorphonuclear leukocytes or
excessive quantity of protein.
Lumbar CSF pressure is 70-180mmh20
Increase in white cells -> Meningitis
CSF formation is independent of intraventricular pressure
Increase in protein content -> tuberculosis, meningitis, poliomyelitis
Absorption is proportional to pressure
Yellowness (Xanthochromia) -> old hemorrhage, jaundice, excess of protein
Pressure < 68mmh20 – absorption stops
Blood staining -> Due to needle injury to a vessel (presence of blood) or due to
Absorption of CSF into venous sinuses via arachnoid villi occurs when pressure subarachnoid hemorrhage.
exceeds the venous pressure in sinuses.
•Meningitis
•CSF circulation
Acute infection of meninges.
Foramen of Magendie
Can be bacterial, viral, protozoal and fungal
Subarachnoid space
Foramen of Luschka
In bacterial, tuberculosis. Fungal meningitis glucose content is low or completely
Arachnoid villi disappear.
Ventricles Viral meningitis glucose content is normal.
Veins of cerebral venous sinuses Bacterial meningitis increased count (pleocytosis) of polymorphonuclear cells.
CSF formation in choroid plexus
Viral meningitis and syphilis lead to increased count of lymphocytes. • Receives afferents from other structures involved in planning;
o the Prefrontal, Premotor Cortex & Posterior Parietal Lobe of the
Tuberculosis lymphocyte increase or mixed type.
cerebral cortex – Via Pontine Nuclei
o Basal Ganglia
Functions of the Cerebellum • Afferent information is integrated with existing proprioceptive info, forming a
modified motor plan.
• The modified plan is then sent to the premotor cortex via the Dentothalamic
Pathway (which decussates at the superior cerebellar peduncles)
Spinocerebellum – Vermis & Intermediate Zone of the Cerebellar Hemispheres,

Globose & Emboliform Nuclei
• AKA: Paleocerebellum
• Function: Involved in Muscle Coordination; controls rate, range, force,
direction & correction of movement, hence ensuring precision & accuracy of
movement
• Afferent sensations of:
o Proprioception – Neuromuscular Spindles, Golgi tendon organs send
impulses via Spinocerebellar & cuneocerebellar tracts
o Linear & Rotational Acceleration – From Vestibular apparatus directly
or by relaying at the vestibular nuclei
o Vision – Tectocerebellar tract
• The cerebellum is a part of the Central Nervous System located in the
Are used to create a picture of current motor pattern. The Spinocerebellum
Posterior Cranial Fossa, & is attached to the midbrain, pons & medulla
compares this to the Motor Plan received from the cortex, & makes modifications
oblongata by the Superior, Middle & Inferior Cerebellar Peduncles respectively.
• Afferents pass into the cerebellum via the middle & inferior peduncles. • Vermis – Controls Axial & Proximal Limb Musculature
Efferents pass out via the superior & inferior peduncles. • Intermediate Zone (Paravermal Area) – Controls Distal Limb Musculature
• Cerebellar Functions include: • Efferents pass:
1. Motor Planning o To the brainstem nuclei (e.g. Red Nucleus via the Globose-Emboliform
2. Motor Coordination Rubral Pathway)
3. Maintaining Posture & Balance o Basal Ganglia
4. Maintaining Muscle Tone o Primary Motor Cortex (via Thalamus), then the corticospinal tracts
• Cerebellum controls same side muscles (unlike cerebrum). o Extrapyramidal Tracts – Modify Movement
• These functions are localized as follows:
Vestibulocerebellum – Flocculonodular Lobe, Fastigial Nucleus
Cerebrocerebellum: Lateral Cerebellar Hemispheres & Dentate Nucleus
• AKA: Archaecerebellum, since it is the oldest part

• AKA Neocerebellum as it is phylogenetically the newest part. • Function: Involved in maintaining posture & balance
• Function: Involved in Motor Planning
• Afferents are the same as for the Spinocerebellum

Basal ganglia
• Efferent Pathways:
1. Fastigial-Vestibular Pathway: Fibres pass to the Medial & Lateral A collection of masses of gray matter situated within each cerebral
Vestibular Nuclei, which give rise to the Medial & Lateral hemisphere
Vestibulospinal Tracts respectively. The former controls neck
movements, the latter controls whole body movements. Both Components
Stimulate Extensors, inhibit flexors Caudate nucleus
2. Fastigial-Reticular Pathway: Pontine reticulospinal tracts (uncrossed) Corpus striatum
increases muscle tone (stimulates α & γ motor neurons), while Lentiform nucleus
Medullary reticulospinal tracts decrease muscle tone.
Cerebellum & Learning – Cerebro-Olivo-Cerebellar Pathway Claustrum
Putamen Globus pallidus

• Cerebellum is concerned with learned adjustments that make coordination
easier when a task is repeated. This is known as procedural memory (as
opposed to declarative memory consolidated in the hippocampus). Lesions in Amygdaloid nuclei
the hippocampus don’t affect this type of memory.
Internus Externus
• As a motor task is learned, the task of generating the motor plan shifts from
the prefrontal cortex to the cerebro-cerebellum.
• Climbing fibres from the Inferior Olivary Nuclei are responsible; their activity
increases & the number of collateral fibres increase as a motor pattern is In addition
learnt. Subthalamic nuclei
Substantia nigra Pars compacta
Pars reticularis
Striatum/Neostriatum = Caudate nucleus + Putamen
Functions
1. Planning and organizing voluntary movement
2. Controlled skilled complex movements most of which are performed
subconsciously
Also, most aspects of vocalization and controlled movements of the eye
3. Change the timing and to scale the intensity of movements.
To determine how rapidly the movement is to be performed
To control how large the movement will be
4. Play a role in cognitive process – Cognitive control of motor activity.
Direct pathway
Neurotransmitters
GABA – Inhibitory
Glutamate – Excitatory
Dopamine (Nigrostriatal pathway)

D1 receptor- excitatory
Acetyl choline [Intrastriatal]
D2 receptor - inhibitory
Connections of basal ganglia
Outputs
Inputs
S.N
GPi Pars reticularis

Thalamostriatal [Acts similar to
Corticostriatal GPi]
Thalamus
Connections within basal ganglia Glutaminergic from S.T

nuclei to GPi
GABAnergic from GPe to

Striatopallidal subthalamic nuclei
Nigrostriatal
[Pallidosubthalamic]
Striatum to GPi and GPe
[GABAnergic]
Pars compacta
to striatum
Indirect pathway Effect of substantia nigra on direct and indirect pathways
Direct pathway
●Act of D1 receptors of striarum ∴ Excitatory
∴Stimulate cerebral cortex Excite direct pathway

Indirect pathway Intra striatal pathway
Within striatum there is a balance between dopamine and acetylcholine
They counter balance each other
Dopamine Ach
• If Dopamine > Ach
Less stimulation of striatum and cortex
•If Ach > Dopamine
Act on D2 receptors ∴ Inhibitory to indirect pathway
Less inhibition of cerebral cortex

More stimulation of striatum and cortex
Disorders of basal ganglia
Show both hypokinetic and hyperkinetic features
Hypokinetic features
a) Akinesia -> Difficulty in initialing a movement

Ex: Mask like face
Inability to initiate as well as stop a movement
b) Bradykinesia -> Slow movements
Hyperkinetic features Environment -> dopamine neuron toxins -> Increase incidence in rural areas
a) Chorea -> Quick, irregular, dancing, non-repetitive movements Smoking -> decrease incidence
1. Huntington disease
Drug induced parkinsonism
Autosomal dominant; age 30-50
Degeneration of GABAnergic fibers of GPe Drugs that blovk striatal dopamine receptors (D2)
Less inhibition -> Hyperkinetic features
Symptoms Choreiform movements Ex: Phenolbutyn given for psychotic behavior
Slurred speech
Other drugs that may decrease striatal dopamine
Dementia
Death in 10-15 years Ex: Tetrabenazines
2. Sydenham chorea
Disease of childhood These disappear once the afent is withdrawn
Rheumatic fever, transient and full recovery
b) Athetosis -> Slow writhing movements mostly of distal limbs.
c) Ballismus -> Flailing, intense, violent, involuntary movements Basis of most common symptoms
d) Hemiballismus -> One side of the body, lesion on contralateral side.
1. Hypokinesia
Parkinson’s disease Normal direct pathway ->Excitatory
Substatia nigra -> Inhibit the direct pathway ->Excitation decreased
A progressive disease Therefore Hyokinesia
Due to degeneration of dopaminergic neurons in the substantia nigra pars
compacta Normal indirect pathway -> Inhibitory
Substantia nigra -> Stimulate the indirect pathway -> Inhibition further
Affects nigra striatal dopaminergic system increases
Therefore Hypokinesia.
Low dopamine in striatum
2. Lead pipe rigidity
Leads to hypersensitivity of the dopaminergic receptors in the past synaptic
neurons in the striatum.
Cerebrum
Main neurological features -> eosinophilic, round, cytoplasmic inclusions called
lewy bodies and lewy neuritis.
Etiology
Reticular formation
Genetic – Persons > 50years -> no genetic effect
++ Reticulospinal tract
<50 years ->10% genetic effect
Muscles
Other Direct -> low vitamins, low antioxidants} increased incident
[Tone is maintained]
Wilsons disease -> Cu2+ accumulated -> Parkinson’s occurs in basal ganglia
Parkinsonism -> Less dopamine -> Cerebrum less stimulated -> Decreased no. of NOTE:
impulses to reticular formation -> Increased firing of reticulospinal tract ->
Increased tone of both agonist and antagonist muscles -> lead pipe rigidity. • Supraoptic - ADH
• Paraventricular - Oxytocin
1. Tremor (resting) • Suprachiasmatic - Circardian rhythms
Normal balance between dopamine and Ach is lost • Preoptic - Fever
Ach promotes stimulation of muscles
Alternatively, hyperflexion and hyperextension occurs with over
stimulation (uncontrolled) Circadian rhythms
Resting tremor occurs
1. Body temperature
Treatments 2. Adrenocortical activity
3. Eosinophil count
L-dopa therapy -> Precursor of dopamine. 4. Renal secretions
5. Sleep- wake cycle
Anticholinergics -> Reduces Ach activity Therefore Dopamine and Ach imbalances
get corrected. Supra chiasmatic nucleus receives special afferents from retina for this purpose.
Deep brain stimulation ->Reduces need for L-dopa and other drugs -> reduces
dyskinesia (Side effect of L-Dopa)
Hypothalamic regulation of temperature
Hypothalamus • Normal body temperature:
▪ Oral - 37°C
▪ Scrotal - 32°C
▪ Rectal - 37.5°C
➢ Temperature is higher in evenings.
Heat production Heat loss

• Food ❖ Conduction
• Contraction of skeletal ❖ Convection
muscles ❖ Radiation
• BAT ❖ Evaporation
• Hormones
▪ Epinephrine
▪ Thyroxine
❖ Peripheral receptors in skin Pathophysiology of fever
Lateral
Free nerve
Aδ fibres spinothalamic
endings
tract Bacterial Monocytes/Macro Cytokines(IL 1,6,
endotoxins phages, Kuffer cells interferons)
Hypothalamus Thalamus VPL

Preoptic area of
OVLT(Supra optic
hypothalamus; set Prostaglandin E2
crest)
point elevated
Mechanisms activated by cold
❖ Heat production is regulated by posterior pituitary

1. Shivering Central and
Peripheral Temperature rising
2. Hormones :Epinephrine, Norepinephrine, TSH
receptors signal mechanisms Fever
3. Hunger ( Lateral hypothalamus) the temperature is activated
4. Vasoconstriction below set point
5. Horripilation
❖ Chills: Conscious
Mechanisms activated by heat
❖ Regulated by anterior pituitary

❖ When the pyrogens are removed set point reaches baseline ( normal –
1. Anorexia 37.5°C.
2. Apathy
3. Cutaneous vasodialation ▪ Heat generation reduces ( Apathy, Anorexia)
4. Sweating ▪ Heat loss increases ( Sweating )
Increased respiration
Internal capsule
Blood supply of the internal capsule
1. Anterior limb
a) Upper part -> Lenticulostriate branches of middle cerebral
artery [Lateral striate]
b) Lower part -> Recurrent branch (Heubrier artery) of anterior
cerebral artery [Medial striate]
2. Genu
a) Upper part ->Lenticulo striate branches of MCA and ACA
b) Lower part -> Direct branches of internal carotid
Heubner artery of ACA
3. Posterior limb
a) Upper part -> Lenticulostriate branches of MCA
b) Lower part -> Anterior chroidal artery (Branch of ICA)
4. Sublentiform
Striate branches from PCA and anterior choroidal
5. Retrolentiform
Striate branches from PCA
❖ Learning and memory:

Higher functions of Nervous system
• Learning - Acquiring information that allows alteration of behavior
based on past experience.
• Memory – Retention and storage of said information.
❖ Higher functions
• Learning
• Memory ❖ Memories are created by groups of neurons in many parts of cortex that
• Language fire together in the same pattern on activation by various stimuli.
• Speech ❖ Links are formed by long term potentiation.
❖ Cognition: Mental process by which humans acquire and use knowledge to Forms of memory
solve problems.
1. Short term (lasts seconds to hours)
• Processing in hippocampus – long term changes in synaptic
strength.
❖ Forebrain: • Disrupted by trauma / drugs
a) Neocortex : Planning, Sensory processing, Thinking, 2. Long term (Resistant to disruption)
Reasoning • Structural changes in synapses ( eg: increased neurotransmitter
b) Limbic system : Emotions, Learning, Memory release, no. of presynaptic terminals and no. of synaptic
connections.
• Occurs in various parts of neocortex.
❖ Neocortex:
a. Frontal : Plan and execute motor functions, Elaborate Molecular basis of memory
thought, Initiative, Judgement, Personality
❖ Alterations in the strength of selected synaptic connections ( e.g. Increased
b. Parietal : Processing of general sensation
protein synthesis and gene activation )
c. Temporal : Processing auditory information and spoken ❖ Occurs in conversion of short term memory to long term memory.
Language
❖ There is inter cortical transfer of memory.
d. Occipital : Processing visual information
❖ Hippocampus : Consolidation ( conversion of short term memory to long
term memory )
❖ 3 functional areas of cerebral cortex Memory disorders

i. Motor areas
❖ Anterograde amnesia
ii. Sensory areas Unable to establish new long-term memories: Damage to
iii. Association areas
hippocampus.
(Conscious behavior involves all 3 areas)
❖ Retrograde amnesia
Inability to recall memories immediately before occurrence of a
traumatic experience. ( eg. Concussion, Electric shock therapy )
Not enough time for consolidation. ❖ Neural plasticity represents forms of learning and memory.
❖ Alzheimer’s disease
Neurogenesis
• Progressive loss of short term memory.
• General decrease of cognitive function – death in middle age. ❖ New neurons form from stem cells in olfactory bulb and hippocampus.
• Intracellular neurofibrillary tangles and extracellular β amyloid ❖ Growth of new granule cells in dentate gyrus of the hippocampus –
plaques. contributes to learning and memory.
❖ Senile dementia Lateralization of brain functions

Alzheimer type memory loss in elderly. 1) Left cerebral hemisphere: Categorical/ Dominant
(sequential – analytical process)
• General interpretive and speech centers, language skills.
• Analytical tasks: Mathematics and logical decision making.
Neural plasticity (Left C.H. dominant in 96% of right handed and 70% of left handed population)
❖ Short/ long term changes in synaptic function based on use/ disuse.
❖ Occurs during childhood development as a response to injury.
2) Right cerebral hemisphere: Representative/ Non dominant
(visual and spatial relations)
• Stereognosis: Identification of objects by form.
1) Post tetanic potentiation
Temporary enhancement of postsynaptic potentials in response to • Recognition of faces and music.
stimuli. Therefore Ca2+ accumulate in presynaptic neurons. (Storage and recognition of faces – Right inferior temporal lobe)
2) Habituation
Repeated neural stimuli evoke decreasing electrical responses.
Lesions in Representative cerebral hemisphere
( Ca2+ channel inactivation )
❖ Agnosia : Inability to recognize an object by a particular sensory modality
3) Sensitization even though that modality is intact
Stronger post synaptic response developed when habituated stimulus is E.g. :- Astereognosis
paired with a noxious stimulus.
❖ Unilateral inattention and neglect: lesion in inferior parietal lobe; neglects
4) Long term potentiation ( LTP ) stimuli from the contralateral side of the body.
• Involves protein synthesis and growth of presynaptic and post
synaptic neurons and connections. ❖ Defects in communication.
• Occurs in hippocampus in formation of long term memories. • Inability to comprehend tone and ‘colour’ of speech.
5) Long term depression ( LTD )

Reduction of synaptic strength.
o Lesion in Broca’s area.

o Slow speech, very little words.
Speech physiology • Fluent/ Receptive aphasia
o Lesion in Wernicke’s area
Can speak, talks excessively, but
nonsense. Can’t understand spoken
or written words.
o Conduction aphasia: Lesion in arcuate

fasciculus
Speech and comprehension
intact. Can’t put words together or
make words.
• Anomic Aphasia/ Dyslexia

o Lesion in Angular gyrus of categorical
hemisphere.
o Difficulty in understanding written
words and pictures. (Visual
information not processed)
o No problem with speech and
❖ Wernicke’s area : Comprehension of auditory and visual language. understanding auditory information.
❖ Broca’s area : Process information from Wernicke’s area into a • Global aphasia
motor pattern for vocalization. o General aphasia involving both
❖ Arcuate fasciculus: Send impulses from Wernicke’s area to Broca’s area. receptive and expressive aspects.
❖ Angular gyrus : Processes information from written words such that o More common than isolated speech
They can be converted to auditory form by disorders.
Wernicke’s area.
❖ Vocalization: ❖ Writing is abnormal in all types of Aphasia.
• Phonation : vocal cords. ❖ Sign language of deaf people is also impaired by lesion in categorical
• Articulation : Lips, Tongue, Soft palate hemisphere.
❖ Lesions of representational hemisphere also have effects – Unable to
Language disorders joke/ tell stories.
1. Aphasia:
Abnormality in language function that is not due to defects of
vision, hearing or motor paralysis. 2. Stuttering
(Caused by lesion in the categorical hemisphere) • Associated with right cerebral hemisphere
dominance and over activity of cerebral cortex and
• Non- fluent/ expressive aphasia cerebellum.
E.g.: - in supplementary motor area • Child : 10 – 12 hours

• Adults : 7 hours
3. Dysarthria
•Difficulty in articulation; impaired muscle Sleep stages
movement of lips, tongue, soft palate – REM and NREM; NREM has 4 stages. (NREM = slow wave sleep)
Unintelligible speech.
E.g.: - scanning speech in cerebellar disorders • 1st enters NREM sleep, spends 70 – 100 minutes in stage 3 and 4.
Monotonous speech in parkinsonism • REM period follows; Cycle repeats at 90 minute intervals.
4. Dysphonia – vocal cord palsy (Right recurrent laryngeal nerve) • Towards morning, more REM, less stage 3,4 sleep.
• Total: 4 – 6 REM periods per night.
Sleep • REM sleep time:
Neonates 50% and Adults 25%
Non-REM sleep stages:

❖ A state of mental and physical inactivity from which one can be aroused.
1. Drifting sensation
❖ Sleep - wake cycle: Circadian rhythm mediated by Suprachiasmatic nucleus 2. Light sleep
of hypothalamus. 3. Vital signs change: BP, RR, Pulse drops
• Receive information about light- dark cycle via 4. Deep sleep; Difficult to arouse
Retinohypothalamic fibers.
• Efferent: Neural (Sleep wake cycle) and melatonin secretion REM
from pineal gland. • Rapid Eye Movements
• Hypothalamus, Reticular formation, Thalamus and cerebral • Vital signs (HR, RR, BP) increase
cortex are involved too. • EEG resembles an awake pattern
• Vivid dreams and penile erections
❖ Restorative effect:
• After the second cycle, REM duration increases
➢ Brain glycogen levels increase.
➢ Memories strengthened, synaptic connections reinforced/
eliminated.
REM NREM
❖ Maintenance of the waking state High threshold for arousal Low threshold
Hypotonia, Twitching movements, No Hypotonia or twitching
• Ascending Reticular activating system; collection of neurons in
Rapid eye movements. movements.
brain stem and diencephalon.
Blood pressure increases Blood pressure decreases
• System is nonspecifically activated equally by different sensory
Irregular pulse Regular pulse
modalities. Dreams more visual, easily recalled Dreams are not readily recalled
• Afferents from Auditory, Visual, Olfactory and Trigeminal EEG desynchronization (Awake EEG synchronization
systems projected to cerebral cortex. pattern)
❖ Sleep requirement:
• New born : 16 – 20 hours
❖ Sleep assessment:
• Electroencephalogram ❖ But threshold for arousal by sensory stimuli and RAS is elevated.
• Electrooculogram (Eye movements)
• Electromyogram (Muscle tone) ❖ Hypotonia of skeletal muscles of neck occurs during REM sleep.
EEG
Sleep Deprivation/ Insomnia
Records voltage changes from postsynaptic potentials in cerebral cortex by scalp
electrodes on skull. • Insufficient or non-restorative sleep despite adequate opportunity to
sleep.
• Brain waves: 4 types • Symptoms
1. α (Alpha): 8 – 13 cycles/ second ✓ Drowsiness
o Most prominent ✓ Fatigue
o When awake but at rest (mind wandering, eyes closed) ✓ Irritability
o Regular, synchronized, larger waves ✓ Reduced concentration and motor activity
2. β (Beta): 13 – 30 Hz
Narcolepsy
o Replaces α (Alpha block) when attention is focused.
o Awake, alert, eyes opened • Chronic neurological disorder; brain unable to regulate sleep – wake cycle
o Asynchronous, low voltage waves normally.
3. Delta • There may be sudden loss of voluntary muscle tone (Cataplexy)
o Stage 3 and 4 of NREM sleep • Go to REM sleep directly from awake state.
4. Theta
❖ Presence of Delta and Theta waves during sleep is normal but presence of Pavo Nocturnus (Nightmares)
these waves when awake is pathological.
❖ Both Delta and Theta are high amplitude, slow waves. • In NREM sleep
Somnambulism – Sleep walking
❖ Brain waves in NREM sleep: • In NREM sleep

✓ Stage 1 : Alpha and Theta • Walk with eyes open and avoid obstacles, cannot recall.
✓ Stage 2 : k complexes and sleep spindles
✓ Stage 3 : < 50% Delta Obstructive sleep apnea
✓ Stage 4 : > 50% Delta • Most common cause of day time sleepiness.
o Failure of pharyngeal muscles to relax/ tongue falls back
❖ REM – Similar to stage 1 (Alpha and Theta) during inspiration.
❖ High amplitude, slow waves of deep sleep are replaced by rapid, low
• Result:
voltage EEG. (Like stage 1/ awake state). Therefore called paradoxical
o Frequent arousal to reestablish respiratory tone.
REM.
o Slow wave sleep reduced (NREM 3 and 4) reduced, 3. No motor response – Loss of muscle tone and absence of tendon reflexes
higher stage 1 sleep.
Apnea test
Coma
This is a crucial test
• Loss of consciousness from which arousal cannot be elicited.
The patient is checked for involuntary respiratory movements
• Disruption of connections between ascending RAS and Thalamus.
The patient is removed from the ventilator machine and before that 100% oxygen is
Brain Death given before breathing
• Brain cannot achieve consciousness. This will prevent hypoxic drive by preventing peripheral chemoreceptor stimulation
• Irreversible loss of brain stem functions.
The co2 level in the blood will rise gradually stimulate the cenral chemoreceptors
• Diagnosis:
and stimulate respiration.
✓ Apnea and deep coma(6 – 12 Hz) – irreversible damage to brain
✓ Absence of brainstem reflexes: Light, Corneal, Gag and Vestibulo – If respiration doesn’t occur until arterial PCO2 is 60mmHg- Brain death is confirmed
ocular reflexes.
✓ Crucial test: No respiratory movement after disconnecting from Facial response to pain
ventilator; PaCO2 rises above 60mmHg Afferents – Via trigeminal nerve to the medial longitudinal fasciculus
✓ No EEG activity
Efferent – Via facial nerve – cause facial muscle contraction
The importance of confirming brain death
Caloric test
1. Spare unnecessary expenditure
2. Give the dignity of death to the patient Check for nystagmus
3. Save the agony of the family
- When cold water is put to the ears eys move to the opposite side
The tests to confirm brain death are - When warm water is put, eyes move to the same side
- Afferents – Via vestibular nerve to the brainstem
1.Apnoea test - Efferents – Via oculomotor nerve
2. Absence of reflexes (Mnemonic: COWS: cold opposite warm same)
a. Light reflex Vestibulo-ocular reflex
b. Corneal reflex When the patients head is held and passively moved to one side suddenly, the
c. Gag reflex patients eye balls move to the opposite side to keep the gaze constant.
d. Facial response to pain Afferents- Via vestibular nerve ( Endolymph of semi circular canals stimulate)
Efferents-Via oculomotor nerve.
e. Caloric test
If there is brain death- the eye balls with the head as the reflex is lost.
f. vestibulo-occular reflex
Anatomy
Brain stem
Mid brain
a) Weber syndrome
Affected side Consequences

Occulomoter nerve fibres Ipsilateral 3rd nerve palsy
Corticospinal fibres Contralateral hemiparesis
b) Benedicts syndrome
Affected site Consequences
Syndromes Weber syndrome
Occulomoter nerve fibres Ipsilateral 3rd nerve palsy
Benedicts syndrome Red nucleus Contralateral termor
Medial leminiscus Contralateral hemiataxia
Pons Syndromes Millard Gabler syndrome/ventral pontine syndrome
Cranial nerves 6,7 palsies corticospinal tract weakness

Medulla oblongata Syndromes: - Lateral medullary syndrome
(PICA Syndrome/Wallenberg syndrome)
Affected side Consequences

a) The vestibular nuclei Nystagmus Nausea Vomiting
Vertigo
b) Inferior cerebellar peduncle Ipsilateral cerebellar signs
c) Nucleus ambiguous of Ipsilateral laryngeal pharyngeal
CN9,10,11 palatal hemiparalysis
Dysarthria Dysphagia Dysphonia
d) Glossopharyngeal nerve roots Loss of gag reflex
e) Spinal trigeminal nucleus and Ipsilateral loss of pain and
tract temperature sensation of the
face
f) Descending sympathetic tract Ipsilateral Horners syndrome
Ptosis miosis anhidrosis
apparent enophthalmos
Hiccups
g) Spinothalamic tracts (spinal Contralateral loss of pain and
leminiscus) temperature sensation of trunk,
upper limbs and lower limbs
Syndrome Medial medullary syndrome/ Dejerine syndrome (anterior Cranial nerves and lesions
spinal artery territory)
12 cranial nerves
1. Sensory only – 1, 2, 8
2. Motor only – 3, 4, 6, 11, 12
3. Mixed – 5, 7, 9, 10
Only four parasympathetic nuclei are involved in cranial nerves
1. Edinger-Westphal nucleus (Oculomotor)

2. Superior salivatory nucleus (Facial)
3. Inferior salivatory nucleus (Glossopharyngeal)
4. Dorsal nucleus (Vagus)
Sympathetic supply to the cranial nerves is by postganglionic fibres from

superior cervical ganglion
1. Olfactory Nerve
Affected side Consequences Peripheral process(olfactory hairs) of bipolar olfactory receptor nerve in the
a) Hypoglossal nucleus Ipsilateral; flaccid paralysis of the neuroepithelium located in the upper part of the
tongue nasal cavity above superior concha (1st Order Neuron)
b) Corticospinal tract Contralateral spastic hemiparesis
c) Medial leminiscus Contralateral loss of tactile and
vibration from the trunk and Central processes of olfactory receptor nerves gather to about 20 olfactory
extremities. filaments
Pass through the cribiform plate and pierces the arachnoid and dura mater
Enters anterior cranial fossa
Forms the Olfactory bulb by synapsing at the anterior end of Olfactory tracts
Axon of 2nd Order neuron pass through the olfactory tract in the olfactory from optic chiasma to the lateral geniculate body
sulcus and reaches the anterior perforated substance
3rd Order neurons project as the optic radiation through the retrolenticular
part of Internal Capsule
Divides into two as lateral and medial striae
Lateral Stria – makes connections with Uncus Terminates in the Visual cortex
Medial Stria – makes connections with other parts of 3. Oculomotor Nerve
limbic system
Two Motor Nuclei
• Olfactory pathway reaches olfactory cortex without relaying in the

thalamus Main motor nucleus Edinger- Westphal Nucleus
(Parasympathetic)
2. Optic Nerve Emerges on the medial surface of base of cerebral peduncle of midbrain
Rods and cones activate bipolar cells in the retina (1st Order)
Passes forward between Posterior Cerebral Artery and Superior Cerebellar
Artery
Their central processes activate ganglion cells in the retina (2nd Order) And then below the Posterior communicating artery
Central processes of ganglion cells converge at optic disc to form the optic Enters the Cavernous Sinus through its roof and continue in the lateral wall
nerve and passes through the meninges of brain and Optic canal
Slants down medial to the Trochlear and Ophthalmic nerves at the anterior
Two optic nerves merge and form the Optic Chiasma above the pituitary part of Cavernous Sinus
gland (Nasal fibres decussate here)
Branches into two at the anterior pole of cavernous sinus and passes
Optic tract projects around the midbrain through Superior Orbital Fissure and then the Tendinous Ring
Superior division Inferior division

Supplies Superior Rectus and Smooth muscle Supplies Medial, 5. Trigeminal Nerve
Inferior Recti
Part of Levator Palpebrae Superioris and Inferior Oblique Mesencephalic Main sensory Spinal nucleus and tract
muscles Motor nucleus
nucleus nucleus
• Parasympathetic fibres to the Sphincter Pupillae and Ciliary muscles

pass through branch to the Inferior Oblique of Inferior Division
Sensory root, emerges from ventral aspect of Pons at the junction with
4. Trochlear Nerve SCP
Nucleus in the midbrain at the level of Inferior Colliculus
Together pass below Tentorium Cerebelli to mouth of Trigeminal Cave

Emerges from the posterior aspect of Midbrain (Only nerve to emerge from
the posterior surface of brainstem) Crosses the upper border of Petrous bone near its apex and passes
from posterior to middle cranial fossa
Immediately decussate with the nerve of opposite side

Motor root remains Sensory root expands and
separate below the ganglion form Trigeminal ganglion
Passes around the Cerebral Peduncle between the Posterior Cerebral and
Superior Cerebellar arteries
Passes through foramen From anterior half; 3 sensory
Ovale divisions
Passes in the Lateral wall of Cavernous Sinus after entering through the roof Mandibular, Maxillary,
Joins with Mandibular nerve Ophthalmic
after passing
Continues forward 1st below the Oculomotor and then above it at the Through foramen ovale
anterior pole of Cavernous Sinus
Mixed Mandibular nerve

Enters the Superior Orbital Fissure lateral to the Tendinous Ring
Passes medially over the Levator Palpebrae Superioris and supply Superior
Oblique
a) Ophthalmic Nerve 1. Zygomatic Nerve – Divides into two after passing through Inferior Orbital
Runs forward in the lateral wall of Cavernous sinus; at its posterior Fissure
end below Trochlear Nerve and Above Maxillary nerve
Sym. Fibres join a) Zygomaticofacial – Perforates facial surface of zygomatic bone and supplies skin
Passes below Trochlear and above Oculomotor nerve at the anterior over the bone
end of Cavernous Sinus b) Zygomaticotemporal – Perforates temporal Surface of Zygomatic bone and
supplies skin above zygomatic arch
Lacrimal Nerve Frontal Nerve Nasociliary nerve 2. Posterior Superior Alveolar – 2/3 branches emerge from Pterygomaxillary fissure
and supply Maxillary Sinus, adjacent gum and Vestibule
Upper part of lateral wall Passes forward above Runs through 3. Infraorbital –
Of orbit Levator palpebrae S. tendinous ring • Emerges through Infraorbital foramen after passing along the floor of
Orbit
• Divides into Anterior Superior Alveolar (supplies canine and 2 incisiors) and
Middle Superior Alveolar Nerve (Supplies premolar teeth)
4. 2 Ganglionic branches – Connect Maxillary and Pterygopalatine ganglion
c) Mandibular Nerve
Mixed nerve in Infratemporal fossa
Between upper head of lateral pterygoid and tensor palati; here otic ganglion lies
on the medial aspect of the nerve
Meningeal branch
Nerve to Medial Pterygoid
Divides into Anterior and Posterior Divisions

1. Anterior Division
a) 2 Nerves to Lateral Pterygoid – One to each Head
b) 2 deep Temporal Nerves – Passes above upper head of Lateral Pterygoid to deep
surface of Temporalis
c) Nerve to Masseter – Passes laterally through Mandibular Notch and sink into
Masseter after giving a branch to Mandibular Joint
d) Buccal Nerve – Only Sensory branch of Anterior Division, emerges between 2
heads of Lateral Pterygoid and pierces Buccinator to supply mucous membrane
deep to Buccinator, vestibular gum of 3 mandibular molar teeth
2. Posterior Division 6. Abducens Nerve

a) Auriculotemporal 2 roots pass back around Receives secretomotor fibres
Nerve Middle Meningeal A. from Otic ganglion Motor Nucleus situated in the Facial Colliculus in the Pons
Ascends behind the joint amd superficial Passes deep to the neck of
mandible Emerges from the anterior lower border of Pons above the Pyramids of Medulla
Temporal Vessels
TMJ major sensory supply
Enters the Pontine Cistern and passes upwards piercing Arachnoid and Dura Mater
Supplies Parotid gland, External Acoustic Meatus, External Surface of Auricle
b) Lingual Nerve Joined by Chorda Deep to lower border of Lateral Pterygoid
Tympani
Passes over the apex of Petrous Temporal bone
Passes under free lower border Infront of Inferior Curves down on medial
Of Superior Constrictor Alveolar Nerve Pterygoid
Runs forward above Mylohyoid Crosses Submandibular Ascends on Enters and continues forward in the Cavernous Sinus inferolateral to the Internal
Duct from lateral to medial Hyoglossus Carotid Artery
Below the duct
Supplies taste to anterior 2/3rd via Chorda tympani, common sensation to anterior Enters the Superior Orbital Fissure and passes through the Tendinous Ring
2/3rd , Submandibular ganglion
c) Inferior Alveolar Passes deep to lower head On lateral surface of Medial Supplies the Lateral Rectus
Nerve of Lateral Pterygoid Pterygoid
Runs in mandibular Enters Mandibular Foramen Lies between Mandible 7. Facial Nerve
Canal Infront of its artery and vein and sphenomandibular
ligament
Main Motor Nucleus Parasympathetic Nucleus Sensory Nucleus
(Superior Salivatory, Lacrimal)
Ends as Incisive and Mental Gives Nerve to Mylohyoid
Branches
➢ Incisive Branch – Supplies both surfaces of lower lip, adjacent gum Lies in the Pontine Posterolateral to main motor Upper part of
and Labial Glands Nucleus Nucleus of Tractus Solitarius
➢ Mental Branch – Supplies Mylohyoid, Anterior Belly of Digastric Reticular Formation
and Small area of Submental Skin after emerging through Mental
Foramen
Emerges at lower border Emerges between Pons and
Of Pons above Olive and ICP (Nervus Intermedius)
Passes laterally in cerebellopontine angle through Pontine Cistern 8. Vestibulocochlear Nerve
Hair cells of Spiral Organ in Internal Hair cells in maculae of Utricle (Static
Enters the Anterosuperior quadrant of Internal Acoustic Meatus Ear (Hearing) Balance) and Saccule and ampullae of
semicircular ducts (Kinetic Balance)
Passes laterally in the Petrous bone above Internal Ear

Cell bodies in the spiral ganglion in Peripheral processes join two parts of
Makes a sharp posterior bend called Geniculum near medial wall of middle ear the base of Spiral Lamina Vestibular part
(containing cell bodies of taste fibres forming Geniculate Ganglion)
Runs back in medial wall of Middle Ear Gives off the Greater Petrosal nerve with Central processes run along the Superior Division – through posterosuperior
below the promontory and above the Nervus Intermedius Fibres Modiolus of Cochlea quadrant
buldge by Lateral Semicircular Canal Inferior Division – through posteroinferior
Emerges from anterosuperior surface of quadrant
Curves downwards over the posterior Petrous Bone in Middle Cranial Fossa Joins with many small nerves and
Wall of Middle Ear Enters the anteroinferior quadrant
Travels in a groove on the bone beneath Of fundus of Internal Acoustic Meatus Cell bodies of 1 st order neuron form the
Gives off Nerve Trigeminal Ganglion and reaches (Cochlear nerve) vestibular ganglion
To stapedius foramen lacerum
Central processes form the vestibular

Passes out through Chorda Tympani Joins Deep Petrosal Nerve and Form Nerve
Stylomastoid foramen Nerve to pterygoid canal
(Sym+Parasym)
Pass through Posterior Two join and form the vestibulocochlear nerve
Wall of Middle Ear Passes through Pterygoid Canal and
enters pterygopalatine ganglion
Passes through pontine Cistern and enters the brainstem through
Passes forward crossing a groove between Pons and Medulla
Neck of Malleus and Tympanic Membrane
Leaves through anterior wall and
Extracranial Branches Emerges through petrotympanic fissure Nerve fibres enter the Vestibular Nuclear complex and Cochlear Nuclei
- Posterior Auricular
- 5 branches in Face Passes down and forwards and join Lingual Cochlear Nuclei Vestibular Nuclear Complex
- Nerves to Stylohyoid nerve in infratemporal fossa
and Digastric Posterior Belly
9. Glossopharyngeal Nerve
Two Nuclei – Anterior,Posterior four nuclei- Superior, Inferior,
Lateral, Motor nucleus Inferior Salivatory nucleus NTS Somatic sensory nucleus
Medial (NA)
Axons pass thorugh Pons to Trapezoid From Lateral – Vestibulospinal Tract

body and Olivary Nucleus From all – Fibres pass to Vestibular
area Emerges from medulla between olive and ICP in a series of rootlets
Relay in the Trapezoid body and Olivary Runs laterally in the Pontine Cistern and enters the anterior compartment of
Nucleus Jugular foramen
Axons form Lateral Lemniscus through Lies lateral to the Inferior Petrosal Sinus and pierces Arachnoid and Dura mater
midbrain
Has small Superior and large Inferior ganglion which notches the inferior border of
Terminate either in Petrous bone just below Internal acoustic Meatus
Medial Geniculate Nucleus of Inferior Tympanic branch

Body Colliculus Passes laterally between Internal Jugular vein and Internal Carotid Artery
Passes into middle ear

Acoustic Radiation through Through tympanic canliculus
Sublentiform part of Internal Capsule Pharyngeal Nerve to
Between Jugular fossa and Carotid Branch branches Stylopharyngeus
Carotid Canal
Auditory Cortex Carotid Sinus Pharyngeal Gives off as it winds
Forms tympanic plexus and body Plexus around the muscle
(Only Muscular branch)
Lesser Petrosal nerve on the
Floor of Middle Cranial Fossa
Passes through Foramen Ovale
Joins the Otic ganglion
Parotid Gland
10. Vagus Nerve

Glossopharyngeal nerve enters the pharynx between Superior and Middle
Constrictors Motor Nucleus Dorsal vagal nucleus NTS Sensory nucleus of Trigeminal
(NA)
Two branches
1. Tonsillar branch – afferent for Tonsillar Mucosa
2. Lingual branch – Common sensation, taste of posterior 1/3rd of tongue and Leaves medulla in a series of rootlets below the 9th CN in the sulcus between Olive
Secretomotor to lingual glands and ICP
Enters Middle Compartment of Jugular Foramen with 11th CN

Meningeal branch (C1,C2)
Auricular Branch Small Superior Ganglion
Cranial root of 11th CN
Long Inferior Ganglion in Jugular Fossa below the Skull base
Enters neck and lies vertical in the Carotid Sheath
Passes in the gutter between Internal/Common Carotid artery and Internal Jugular
Vein
Baroreceptors and chemoreceptors in Aortic Arch
Pharyngeal Branch Passes between Internal Both motor and Sensory
And External Carotid A. to Pharyngeal Plexus
Superior Laryngeal Internal Laryngeal – Motor to Cricothyroid
Branch runs deep to External Laryngeal Pierces thyrohyoid membrane
Carotids Sensory to Laryngeal Mucosa
Upto Vocal Folds and Pharynx
Central Cardiac Right Upper and Lower Deep Cardiac Plexus
Branches Left Upper
Lower Superficial Cardiac Plexus
Recurrent Left R. Hooks around Ascends In tracheo-

Laryngeal ligamentum arteriosum oesophageal groove
Right R. Hooks under Subclavian

Runs up in Tracheo-oseophageal 11. Accessory Nerve

Groove
Axons of nerve cells of NA Axons of nerve cells in Anterior Horn of
(Cranial Root) upper 5/6 cervical segments of Spinal Cord
Passes under Inferior Constrictor
(Spinal Root)
Behind Cricothyroid joint
Emerges from the midbrain as a
Series of rootlets between Olive Emerges as a series of rootlets from the
Supply laryngeal muscles (except
And ICP lateral surface of Spinal Cord behind the
Cricothyroid), Laryngeal Mucosa
Denticulate ligament
Below Vocal folds, Cricopharyngeus,
Cardiac branches
Forms a single nerve and ascends
In Superior Mediastinum passes infront of Subclavian Artery
2 roots unite and pass through middle compartment of Jugular Foramen

Right Vagus – Comes into contact with Trachea posterior to SVC
Left Vagus – Lies between Left Common Carotid and Subclavian Arteries (No contact Gives all fibres of Cranial root to Nerve runs downwards and
with Trachea), crosses the left side of Aortic Arch backwards
Vagus Nerve across Internal Jugular vein passing
Passes behind the lung roots Infront of Transverse process of Atlas
Supplies Striated muscles of
Breaks up into branches and form Oesophageal Plexus Soft palate and Larynx Supplies Sternocleidomastoid and
Trapezius
Anterior Vagal Trunk
Posterior Vagal Trunk 12. Hypoglossal Nerve
Enters abdomen through Oseophageal Opening and Suppy Stomatch, foregut, Nucleus in the Medulla
midgut, Biliary tract, Pancreas
Emerges from series of rootlets between Pyramid and Olive in Medulla
2 roots join and pass through the hypoglossal canal in Occipital Bone
Nerve passes down between Internal Jugular Vein and Internal Carotid Artery
Nerve swings forward crossing both carotid arteries and loop at the Taste Pathways
commencement of the lingual artery
Passes superficial to the Hyoglossus muscle

Soft Palate Anterior 2/3rd Posterior 1/3rd Epiglottis
of Tongue of Tongue
Supplies all the muscles of Tongue except Palatoglossus
Gives off Superior root of Ansa Cervicalis Lesser Palatine Lingual Nerve Lingual branch Vagus Nerve
Nerves of 9th CN
Lies in the anterior wall of Carotid Sheath under
The cover of Sternocleidomastoid Pterygopalatine Chorda Ganglion of
Ganglion Tympani 9th CN
Nerve to Pterygoid Facial Nerve 9th CN

Canal
Greater Petrosal
Nerve
Geniculate
Ganglion
Facial Nerve
Nucleus of Tractus Solitarius

Parasympathetic Pathways Cranial Nerve Lesions

1. Superior Salivary Nucleus Nervus Intermedius Chorda Joins Lingual
Cranial Nerve Condition Causes
of Facial Nerve Tympani Nerve
Anterior Lingual Gland
Secretomotor to glands in floor of mouth Submandibular
1. Olfactory Nerve Bilateral Anosmia Disease of the
Submandibular and sublingual glands ganglion
Olfactory Mucous
Membrane
2. Inferior Salivary Nucleus 9th CN Tympanic Tympanic Lesser Eg- Common Cold,
Branch Plexus Petrosal N. Allergic Rhinitis
Parotid Gland Auriculotemporal nerve of 5th CN Otic ganglion

Unilateral Anosmia Disease affecting the
Olfactory bulbs or tract
3. Lacrimatory Nucleus Facial Greater Nerve to Pterygoid Pterygopa-
1. Fractures of
Nerve petrosal N. canal -latine ganglion Anterior
Cranial Fossa
Lacrimal N. Zygomaticotemporal N. Zygomatic nerve Maxillary involving
Cribiform
nerve
Plate of
Lacrimal Gland Ethmoid bone
Damage to
4. Edinger- Westphal Nucleus Oculomotor Inferior Nerve to Inferior Olfactory
Nerve
Nerve Division Oblique
2. Tumors of the
Frontal lobe
Constrictor Pupillae, Ciliary muscles Short Ciliary Nerves Ciliary Ganglion or
meningiomas
of Anterior
Cranial Fossa
Presses on
Olfactory
bulbs or tract
2. Optic Nerve Circumferential Hysteria
Blindness Optic Neuritis – occur
following spread of
infection from the
Ethmoid and Sphenoid
Sinuses
Total Blindness of One Complete section of 4. Trochlear Nerve Double vision on looking Paralysis of Superior
eye One Optic Nerve straight downwards Oblique muscle (Eye
Nasal Hemianopia Partial lesion of the turns medially and
Optic Chiasma on its downward)
lateral side Conditions leading to
Bitemporal Hemianopia Sagittal section of Trochlear Nerve
Optic Chiasma Damage
Most commonly 1. Cavernous
produced by tumor of Sinus
the Pituitary gland Thrombosis
Contralateral Division of Optic tract 2. Aneurysm of
Homonymous or Optic Radiation Internal
Hemianopia Destruction of the Carotid Artery
Visual Cortex on one 3. Vascular
side (same hemianopia lesions of the
for both eyes) dorsal part of
3. Oculomotor Nerve Inability to move the Complete lesion of Midbrain
eye upward, downward Oculomotor Nerve 5. Trigeminal Nerve Deviation of Jaw to one Paralysis of muscles of
or inward At rest eyes look side upon protruding mastication specially
1. laterally – due to Lateral Pterygoid
unopposed activity of muscle
lateral rectus 6. Abducens Nerve Internal Strabismus Unopposed action of
2. downwards – Medial Rectus due to
unopposed action of paralysis of Lateral
superior oblique Rectus Muscle
Diplopia Inability to converge NOTE – Internuclear Ophthalmoplegia – Lesions
the rays from both of the Medial Longitudinal Fasciculus leading to
eyes to a common axis disconnection of Oculomotor nucleus innervating
owing to paralysis of Medial Rectus from Abducens Nerve innervating
EOMs Lateral Rectus
Ptosis Paralysis of Levator 7. Facial Nerve Loss of taste over Nerve is damaged
Palpebrae Superioris anterior 2/3rd of the proximal to the point
Internal Incomplete lesion of tongue where it gives off
Ophthalmoplegia Oculomotor nerve with Chorda Tympani
selective loss of branch of Facial Canal
autonomic innervation Bell Palsy Dysfunction of Facial
of Sphincter Pupillae Nerve as it lies within
and Ciliary Muscle the facial canal ;
External Paralysis of EOMs with usually unilateral
Ophthalmoplegia sparing of Sphincter Sometimes follows
Pupillae and Ciliary exposure of face to a
muscles cold draft
NOTE – – acoustic
• Fibres innervating the upper facial Neroma,
muscles receives corticonuclear fibres Trauma)
from both cerebral hemispheres - Lesions of the
• In contrast fibres innervating lower facial CNS (Tumors
muscles receives corticonuclear fibres of Midbrain,
from contralateral hemisphere only Multiple
• In UMN type lesion ability to wrinkle the Sclerosis)
forehead remains as Frontalis muscle is
innervated by both cerebral 10. Vagus Nerve Deviation of Uvula to a Unopposed action of
hemispheres unlike in a LMN type lesion side when saying ‘ah’ Palatine muscles due
where it is not possible to paralysis of one side
• In both types of lesions mouth deviate to Uvula deviates to the
the healthy side healthy side
8. Vestibulocochlear Nystagmus Disturbance in the Hoarseness or absence Lesion of Recurrent
Nerve - Uncontrollable reflex control of EOMs of voice Laryngeal nerves
rhythmic which is one of the resulting paralysis of
oscillation of functions of laryngeal muscles
the eyes semicircular canals 11. Accessory Nerve Atrophy of Paralysis of
leading to a Sternocleidomastoid Sternocleidomastoid
fast phase and weakness in turning muscle due to lesion of
which is away of head to opposite side spinal part of
from the side Accessory Nerve
of the lesion Drooping of shoulder Paralysis of Trapezius
Vertigo with difficulty in raising muscle due to a lesion
Deafness - Defect of the arm above the of spinal part
Tinnitus auditory horizontal level Accessory Nerve
conducting 12. Hypoglossal Nerve Deviation of tongue to a Paralysis of
mechanism of side upon protruding Genioglossus muscle of
middle ear one side resulting in
- Damage to unopposed action of
receptor cells the other
in spiral
oragan of
Corti Damaged Nerve Deviating organ Deviating side
- Lesions of the Trigeminal Nerve Jaw Paralyzed
Inner Ear Facial Nerve Mouth Opposite
(Acute Vagus Nerve Uvula when saying ‘ah’ Opposite
Labyrinthitis Hypoglossal Nerve Tongue when protruding Paralyzed
- Lesions of the
Cochlear
Nerve (Tumor
- Interpeduncular cistern
The meninges - Chiasmatic cistern
The meninges are connective tissue membranes that line the skull and the vertebral
Dura mater
canal enclose the central nervous system (The brain and the spinal cord)
The dura mater consists of an outer endosteal layer and an inner meningeal
There are 3 layers:
layer.
1. Pia mater
The two layers are united except where they separate to enclose the venous
2. Dura mater
sinuses.
3. Arachnoid mater
The outer layer is the periosteum of the bone and blood vessels pass through it
Covering the interior of the cranium is the dura mater and covering the brain
to supply the bone.
substance is the pia mater, in between them the arachnoid mater is situated
connected to pia by many fine filamentous processes. Inner layer is of dense fibrous membrane
Pia mater Over the vault of the skull the fused layers can be easily stripped away but over
the base of the skull the layers are firmly attached making it difficult to remove.
It invests the brain and the spinal cord and also contain blood vessels.
It forms several folds/reflections; falx cerebri, falx cerebelli, tentorium
Nowhere does it any structure intervene in between the pia and the brain
cerebelli, diaphragma sellae.
substance.
Blood supply
It is even related to the depths of the deepest fissures and sulci.
The inner layer of the dura requires very little blood to nourish it, the outer
The space between the pia and arachnoid is the subarachnoid space filled with CSF
layer on the other hand is richly supplied.
Dura mater
Arterial supply includes;
It is a delicate membrane supported by the inner layer of dura mater.
The middle meningeal artery, meningeal branches of ophthalmic, ethmoidal,
It is connected to the pia by many filamentous processes hence the name internal carotid, and vertebral arteries, accessory meningeal artery, ascending
“Arachnoid mater” (like a spider’s web) is used. pharyngeal artery, occipital arteries.
Vessels and nerves pierce the dura and arachnoid mater both at the same place; Venous drainage;
they cross the subdural space but do not run along the two membranes.
Much of the blood drained from the marrow is drained by diploic veins that
Arachnoid granulation are herniations in certain areas through little holes in the emerge on the exterior, others drain to venous sinuses. The remaining blood
dura mater to venous sinus through which CSF oozes back into blood. drains in to middle meningeal vein.
Between the base of the brain and base of skull several larger spaces exist as a Innervation
result of the incompatibility of the contour of bone and brain parenchyma.
Innervation is by ophthalmic nerves, ethmoidal nerves, meningeal branches of
They form several subarachnoid cisterns the ophthalmic, maxillary, mandibular, vagus and hypoglossal nerves. The
tentorial branches of the ophthalmic and maxillary nerves and C3 and C4 spinal
- Cerebellomedullary cistern nerves.
- Pontine cistern
Intracranial hemorrhage (bleeding that occurs within the skull)
Outside the Inside brain tissue

brain tissue
•Intra cerebral
•Epidural
•Intra ventricular
•Subdural
•Subarachnoid
•Epidural hemorrhage
Occupies the space between skull and Dural mater
Often due to a result of trauma to head
Usually present with skull fractures as well
Produces a lens shaped collection of blood
Bleeding source mostly arterial
The middle meningeal artery
•Subdural hemorrhage
Occupies the space between the dura mater and

arachnoid membrane
Causes are similar to above
Source is often tearing of bridging veins ∴mainly venous blood
Produces a crescent shaped collection of blood
Most have lucid interval leading to progressive neuro decline and then coma
•Subarachnoid hemorrhage
As the name suggests it occupies the subarachnoid space
Often a result of a cerebral artery rupture, specifically an aneurysm

Most commonly saccular type of aneurysm The contents
Often with a sudden severe thunderclap headache

The contents can be classified as structures that travel through the sinus or those
that travel through the lateral wall of the sinus.
Travels through cavernous Travels through lateral wall of

sinus cavernous sinus
Cavernous sinus • •Abducens nerve (CN VI) • •Oculomotor nerve (CN III)
• •
Lies alongside the body of the sphenoid bone in the middle cranial fossa
• •
•Carotid plexus (post-ganglionic •Trochlear nerve (CN IV)
It contains the Internal carotid artery and cranial nerves. sympathetic nerve fibres) •
• • •Ophthalmic (V1) and maxillary
Each receives blood from 3 sources (Orbit, vault bones, and cerebral hemisphere) • •Internal carotid artery (V2) branches of the trigeminal
(cavernous portion) nerve
Each drain by superior and inferior petrosal sinuses to the sigmoid sinus and
internal jugular vein respectively.
The borders of the cavernous sinus are as follows:
• Anterior – superior orbital fissure.

• Posterior – petrous part of the temporal bone.
• Medial – body of the sphenoid bone.
• Lateral – meningeal layer of the dura mater running from the roof to the floor of the
middle cranial fossa.
• Roof – meningeal layer of the dura mater that attaches to the anterior and middle
clinoid processes of the sphenoid bone.
• Floor – endosteal layer of dura mater that overlies the base of the greater wing of
the sphenoid bone.
Veins of the cavernous sinus

Blood supply of the brain and the circle of Willis
The blood flow in the cavernous sinus can be in either direction depending on the
local venous pressures. There are not valves in the cavernous sinus. Brain is supplied by the two internal carotid and two vertebral arteries
Each cavernous sinus receives venous drainage from: Circle of Willis -> Two arterial systems anastomose with each other around
the optic chiasma and infundibulum of the pituitary stalk forming the circle
• Ophthalmic veins (superior and inferior) – these enter the cavernous sinus via the of Willis. This arterial circle lies within the subarachnoid space.
superior orbital fissure.
• Central vein of the retina – drains into the superior ophthalmic vein, or directly into Two vertebral arteries unite in the midline to form the basilar artery} lower
the cavernous sinus. border of pons.
• Superior petrosal sinus – Leaves the top posterior end of the sinus and enters the
commencement of the sigmoid sinus. Basilar artery divides into two posterior cerebral arteries -> Upper border of
• Inferior petrosal sinus – Empties bulk of the blood from the sinus, leaves the pons
posterior end of the sinus.
• Sphenoparietal sinus – empties into the anterior aspect of the cavernous sinus.
Other branches of the basilar artery except posterior cerebral arteries ->
• Superficial middle cerebral vein – contributes to the venous drainage of the Pontine arteries Labyrinthine arteries Anterior inferior cerebellar arteries
cerebrum Superior cerebellar arteries
• Pterygoid plexus – located within the infratemporal fossa.
Internal carotid artery emerges from the root of cavernous sinus and gives
Clinical significance off the ophthalmic artery and then curls back to lie on the front half of the
roof.
1. Cavernous sinus thrombosis (CST)
The “danger area of the face” comprises the upper lip, nose and Then turns vertically upwards to the anterior perforated substance and
medial part of the cheek. It lies between two veins the angular vein divides into anterior and middle cerebral arteries.
(via superior ophthalmic vein) and deep facial vein (via pterygoid
plexus and emissary vein) that communicate with the cavernous Other branches
sinus. Infection of the skin may spread via these connections and
1. Anterior choroidal artery
produce thrombosis. By the superficial cerebral vein the
thrombosis can spread to the cerebral hemisphere as well. 2. Posterior communicating
3. Striate arteries
2. Rupture of the internal carotid artery within the cavernous sinus

following a fracture of the skull base produces a pulsating
exophthalmos (Bulging of eye ball) from investment of ophthalmic
veins with arterial blood.
Clinical significance: Rupture of an aneurism of the arterial circle

accounts for 90% of subarachnoid hemorrhages. Congenital aneurysms
are more commonly found on the carotid part than the basilar part,
most of them at the junctional sites where vessels branch.
Artery Areas supplied

Choroidal artery Crus cerebri, Lateral geniculate
body, Optic tract, internal
capsule
Anterior cerebral artery Motor, sensory areas for
1. Cortical branches opposite leg, foot and perineum
2. Central branches including micturition and
defecation centers.
Lentiform nucleus, caudate
nucleus, internal capsule.
Middle cerebral artery Motor, sensory areas for
1. Cortical branches opposite half of the body except
leg, foot, perineum
(Supplied by anterior cerebral
artery)
Auditory and speech areas,
macula area
Middle cerebral artery Lentiform nucleus, caudate
1. Central branches nucleus, internal capsule
Posterior cerebral artery Inferolateral and media surfaces
1. Cortical branches of the temporal lobe and lateral
2. Central branches and medial surfaces of the
occipital lobe.
Thalamus, lentiform nucleus,
midbrain, medial geniculate
bodies.
Effects of occlusion of arteries
Artery Effect
Anterior cerebral artery Contralateral hemiparesis,
hemisensory loss involving leg,
foot, perineum.
Inability to identify objects Brain: Sulci and gyri

correctly
Personality changes
Middle cerebral artery Contralateral hemiparesis,
hemisensory loss mainly in face,
arm
Aphasia
Contralateral homonymous
hemianopia
Posterior cerebral artery Contralateral; homonymous
hemianopia with macula sparing
Visual agnosia
Memory impairment
Veins
● Veins have no muscular tissue, thin walls, no walls, no valves.
●They emerge from the brain and lie in the subarachnoid space.
Veins
External cerebral Internal cerebral

1. Superior cerebral - Drains to superior sagittal sinus
2. Superficial middle cerebral
3. Deep middle cerebral
● Deep middle cerebral vein joined by anterior cerebral and striate

veins to form the basilar vein.
● Two internal cerebral veins unite beneath the splenium of corpus

callosum to form the great cerebral vein, which empties into the
straight sinus.
Thalamus Corpus striatum Substantia nigra

Premotor cortex Corpus striatum
Other thalamic Premotor
nuclei cortex
Other thalamic
nuclei
Ventral lateral Similar to above Influences activity
In addition of motor cortex
Major input-
>Cerebellum
Minor input -> red
nucleus
Ventral Trigeminal Primary somatic Relays common
postero leminiscus sensory cortex sensations to
medial (VPM) Gustatory fibers [areas 3,1an2] consciousness
Ventro Medial and spinal Primary somatic “
postero lateral lemnisci sensory cortex
(VPL)
Intralaminar Reticular formation To cerebral Influences level of
Spinothalamic and cortex via other consciousness and
Nuclei Afferent Efferent Function trigeminalthalamic nucleui alertness
Anterior Mammillothalamic Cingulate gyrus Emotional tone tracts Corpus striatum
tract Hypothalamus Mechanisms of Midline Reticular formation
Cingulate gyrus recent memory Reticular Cerebral cortex Other thalamic
Hypothalamus Reticular formation nuclei
Dorsomedial Prefrontal cortex [Same as Integration of Medial Inferior colliculus Auditory Hearing
Hypothalamus afferents] somatic, visceral, geniculate Lateral leminiscus radiation to
Other thalamic olfactory body from both ears; superior
nuclei information and mostly temporal gyrus
relation to contralateral
emotional feelings Lateral Optic tract Optic radiation Visual information
and subjective geniculate to visual cortex from opposite
states body of occipital lobe field of vision
Lateral dorsal Cerebral cortex Central cortex
Lateral Other thalamic Other thalamic
posterior nuclei nuclei
Pulvinar
Ventral Reticular formation Reticular Influences activity
anterior Substantia nigra formation of motor cortex
Limbic system Stria medullaris
- A part of epithalamus
Group of structures in the border between cerebral cortex and
- Contains afferent fibers from septal nuclei, lateral pre optrea
hypothalamus.
hypothalamic region and anterior thalamic nuclei to habenula
Controls emotion, behavior, drive and memory.
Hippocampal formation
Components
Hippocampus: - Gray matter
The hippocampus, fimbria, fornix, dentate gyrus and mammillary body.
- Floor of inferior horn of lateral ventricle
The uncus, the cingulate and the Para hippocampal gyri. - Connecting pathway
Alveus fimbria 2 crura of fornix body of fornix 2 columns of fornix
The amygdaloid body.
mammillary body
The septal and piriform areas of cerebral cortex, near lamina terminalis and Commissure of fornix ->fibers decussate to opposite hippocampus
anterior thalamic nucleus.
Dentate gyrus: - Between fimbria and Para hippocampal gyrus contains
posteriorly with indusium griseum (gray matter)
Para hippocampal gyrus: - Between hippocampal fissure and collateral

sulcus.
Amygdaloid nucleus
- Almond shaped
- Above inferior horn of lateral ventricle
- Fused with tail of caudate nucleus
- Stria terminalis emerges posteriorly
Afferent connections of hippocampus
a) Cingulate gyrus
b) Septal nuclei
c) Other hippocampus
d) Indusieum griseum
Connecting pathways e) Entorhinal area of cortex
Alveus fimbria fornix mammillothalamic tract Anterior f) Dentate and Para hippocampal gyri
thalamic nucleus
Efferent connections of hippocampus (From fornix) Cranial parasympathetic ganglia

a) Mammillary body
The parasympathetic supply of the body is wholly visceral except the supra
b) Anterior thalamic nuclei
renal glands and the gonads as they appear to only have a sympathetic
c) Tegmentum of midbrain
supply.
d) Septal nuclei
e) Habenular nuclei The preganglionic fibers of the cranial origin
NOTE: Hypothalamus is the major output pathway for limbic system. - Edinger Westphal nucleus
- Superior salivatory nucleus of 7th CN
Functions of limbic system.
- Inferior salivatory nucleus of 9th CN
1. Emotionalbehavior:Fear , anger, sex - Dorsal motor nucleus of the vagus
[Via hypothalamus -> ANS and endocrine]
Note: The postganglionic cells for the first three are in the 4
2. Conversion of recent memory to long term memory ->
parasympathetic ganglia of the cranial region, while the vagal fibers synapse
Hippocampus
with postganglionic cell bodies in the viscera supplied (heart, lungs and gut)
•Cranial parasympathetic ganglia

Lesions of limbic system
There are 4 and are very similar in plan
1. Schizophrenia
1. Ciliary
- A mental disorder characterized by abnormal behavior, strange speech
2. Pterygopalatine
and decreased ability to understand reality
3. Submandibular
- Other symptoms False beliefs, Unclear or confused thinking, Hearing
4. Otic
voices that do not exist.
- Treated by blocking dopamine receptors in limbic system. Each has
- Parasympathetic root
2. Destruction of amygdaloid complex.
- Sympathetic root
- Reduces aggression
- Sensory root
- Emotional instability
- Branches from the ganglion to particular to which they supply
- Increased interest in food
- Hypersexuality. Note: Only the parasympathetic preganglionic fibers synapse in the ganglia
while all others simply pass through it.
•Ciliary ganglion
Situated lateral to the optic nerve, between the nerve and the lateral rectus
The parasympathetic root supplies the ciliary muscle and the sphincter •Submandibular ganglion
pupillae
IS situated hanging suspended from the lingual nerve on the surface of
The cell body being in the Edinger -Westphal nucleus and the fibers relay in hyoglossus.
the ganglion and supply the ciliary body for accommodation and the
Parasympathetic are from the superior salivatory nucleus by the nervus
sphincter papillae
intermedis part of the facial nerve and the chorda tympani joining the
The sympathetic root is a branch from the internal carotid plexus lingual nerve.
Sensory root is a branch of nasociliary nerve that supplies the eye but Sympathetic root is from the superior cervical ganglion by fibers running
doesn’t supply the conjunctiva with the facial artery
Branches of the ganglion are 8-10 short ciliary nerves. Sensory from a branch of the lingula nerve with cell bodies in the trigeminal
ganglion
•Pterygopalatine ganglion
The branches are supplying the submandibular and sublingual glands via
Situated immediately Infront of the opening of the pterygoid canal and the
branches of lingual nerve
nerve to that canal runs straight into the back of the ganglion. The ganglion
is related to the maxillary nerve as it is below and medial to foramen •Otic ganglion
rotundum
Lies between the tensor palatini and the mandibular nerve just below the
It is known as the ganglion of hay fever (“Running nose and eyes”) foramen ovale. It is closely applied to the medial surface of the nerve
The parasympathetic for the ganglion are from a branch of the facial nerve This is the relay station for the parasympathetic secretomotor fibers to
called the greater petrosal nerve from the nervous intermediate part of parotid gland.
facial nerve. They supply secretomotor fibers to lacrimal nasal and palatine
Parasympathetic root comes from the inferior salivatory nucleus by the
glands.
glossopharyngeal nerve and its tympanic branch to the tympanic plexus and
The sympathetic are from the deep petrosal nerve from the carotid plexus from there along the lesser petrosal nerve.
These to join to form the nerve of the pterygoid canal (Vidian nerve) which Sympathetic fibers from the superior cervical ganglion by fibers running
joins the ganglion with middle meningeal artery
The sensory root is a branch of the maxillary nerve Sensory from auriculotemporal nerve with cell bodies in trigeminal ganglion
The branches of the ganglion are distributed to nose palate and Branches are to the parotid gland via filament of the auriculotemporal nerve
nasopharynx.
The otic ganglia is an exception in which it also contains a somatic motor
They are distributed through the lateral posterior superior nasal nerves, root from the medial pterygoid to supply the tensor tympani and tensor
greater palatine nerve, lesser palatine nerve and pharyngeal nerve. palatini muscles.
Q: Posture and balance
Posture & Balance

• Balance is the means by which body position (i.e. posture) is maintained
while stationary or mobile, relative to the environment.
Neural Factors Aiding in Balance
1. Sensory Inputs & Afferent Pathways

a) Proprioception – Joint position, muscle tension & length, etc.
Sensed by neuromuscular spindles, Golgi tendon organs & other joint

receptors. Impulses travel via peripheral nerves to the spinal cord.
Afferents pass to the Cerebellum via:
I. Posterior Spinocerebellar Tract – Trunk & Lower Limb

II. Anterior Spinocerebellar Tract – Trunk, Upper & Lower Limbs
III. Cuneocerebellar Tract – Originates from the Cuneate Nucleus
(so it’s an offshoot of the Dorsal White Columns), conveys info
from the upper thoracic & cervical regions
Afferents pass to the cerebral cortex via Dorsal White Columns (Medial
Lemniscus Pathway)
b) Visual Cues – Processed in the Superior Colliculus of the Midbrain. The

Superior colliculus gives rise to the following:
I. Tectospinal Tract – Adjusts posture in response to visual stimuli
II. Tectocerebellar Tract – Conveys visual info to the cerebellum
c) Vestibular Apparatus –
• Utricle (horizontal) & Saccule (vertical) detect linear
acceleration, semi-circular canals detect rotational acceleration.
• Afferents pass from the vestibular apparatus via the
Vestibulocochlear Nerve (Cranial Nerve VIII)
• Impulses pass to the Flocculonodular Lobe of the Cerebellum,
either directly, or after relaying in the vestibular nuclei, as the
Vestibulocerebellar tract.
• All afferents to the flocculonodular lobe pass via the inferior ii. Medial Vestibular Nucleus receives impulses from the
cerebellar peduncle. fastigial nucleus, gives rise to the Medial
d) Exteroception – Touch, pressure, vibration (e.g. from sole of the foot) Vestibulospinal Tract, which causes neck movements
pass via peripheral nerves to the spinal cord, then, to compensate for head movements
• Via Spinothalamic Tracts to the Cerebral Cortex II. Fastigial-Reticular Pathway – efferent from the fastigial nucleus
• Via the Anterior Spinocerebellar Tract to the Cerebellum synapse with neurons in the reticular formation, altering
impulse transmission of pontine & medullary Reticulospinal
Tracts, which alters muscle tone
• To maintain balance, 2 of the 3 main sensory inputs; Vision, Vestibular
& Proprioception must be intact. Exteroception only helps in balance &
is neither necessary or sufficient to maintain balance.
• Romberg’s Test: Patient’s eyes are closed (removing visual cues). He b) Brainstem – Contains important nuclei such has the Red Nucleus,
must then rely on both proprioception & vestibular afferents to Superior & Inferior Colliculi, Vestibular Nuclei & Reticular Formation
maintain balance. If either one of them is impaired, the patient will lose which act as relay centres for impulses to & from the cerebral cortex &
balance, i.e. he will tilt/sway to one side. If this happens, it is a positive cerebellum
Romberg’s test. [NOTE: Cerebellar Lesions will also give a positive c) Basal Ganglia – Promotes movement needed to maintain balance while
Romberg’s test]. inhibiting movements that result in a loss of balance.
2. Central Nervous System – Processing Unit d) Spinal Cord –
I. Monosynaptic Stretch Reflex – Maintains muscle tone & alters
muscle tension in response to movements to maintain posture
• Integrates information from the various sensory modalities, plans & (e.g. leaning forward stretches the calf muscles, which increases
executes motor commands needed to maintain balance. their tone).
• II. Withdrawal Reflex – This is a polysynaptic stretch reflex arc,
a) Vestibulocerebellum – Flocculonodular Lobe & Fastigial Nucleus consisting of 2 parts:
i. Reciprocal Inhibition – Flexor Contraction causes
Integrates sensory info (mentioned above) & sends efferent signals to
extensor relaxation of the same limb
maintain balance via the following pathways:
ii. Cross Extensor Reflex – Flexor Contraction causes
I. Fastigial-Vestibular Pathway extensor contraction of the opposite limb, thus
i. Lateral Vestibular Nucleus receives impulses from the maintaining balance & preparing the body to escape
fastigial nucleus, & in turn gives rise to the Lateral III. Important Descending Motor Tracts – Anterior Corticospinal
Vestibulospinal Tract, which alters muscle tone Tracts (Controls trunk muscles) & Medial Brainstem Pathways
(stimulates extensors, relaxes flexors) to maintain (Tectospinal, Vestibulospinal & Reticulospinal [TVR) Tracts)
balance in response to changes in acceleration of the e) Cerebral Cortex – Role in balance unclear but prefrontal cortex may be
body involved.
3. Effectors – Antigravity Muscles (See below)

Musculoskeletal Adaptations for Maintaining Erect Posture
1. Atlanto-occipital Joint & Neck: Countering the Tendency to Flex
a) Bony – Odontoid process of the axis lies behind the atlas,
secondary curvature of the cervical spine
• Line of gravity – An imaginary line running through the centre of gravity b) Ligaments – Cruciate Ligament holds down the odontoid
of the body; the closer a joint is to the line of gravity, the more stable it process. Ligamentum nuchae is tensed when neck is flexed
is & the easier it is to maintain posture. (antigravity effect)
• The major joints along the body axis lie either in front of or behind the c) Muscular – Neck extensors, mainly Splenius Capitis & Splenius
line of gravity (Ref Snell’s Chapter 3- pg 104): Cervicis
2. Trunk – Countering the Tendency to Flex
a) Bony – Thoracic & Lumbar curvatures (caused by the wedge
shape of the vertebrae & discs) are opposed in direction. Since
they are stacked on each other, helps maintain erect posture
b) Ligaments – Supraspinous (mainly thoracic), Interspinous
(mainly lumbar) ligaments, Ligamentum flava, Anterior &
Posterior Longitudinal Ligaments. The Sacroiliac Ligaments are
the strongest ligaments in the body, which prevents the sacrum
being displaced forwards by body weight.
c) Muscles – Erector Spinae. Tone of anterior abdominal muscles
increase intraabdominal pressure, supporting the body above
3. Hip – Countering the Tendency to Hyperextend

a) Bony – Articulation of the hip joint is such that it acts as a lever
system, transmitting force created in the lower limb to keep the
trunk erect
b) Ligaments – Iliofemoral Ligament lies in front of the hip joint is
the second strongest ligament in the body. Ischiofemoral &
Pubofemoral ligaments also help stabilize
c) Muscles – Short muscles of the hip (Obturators gluteus medius
& minimus, gemelli, quadratus femoris, piriformis, etc.), hip
adductors, rectus femoris (of Quadriceps)
• Joints tend to displace towards the line of gravity. As with all joints,
Bony, Ligamentous & Muscular factors maintain stability & assist in
erect posture.
4. Knee – Countering the Tendency of the Femur to slide forward on the Tibia
a) Bony – Intercondylar eminence of Tibia imparts lateral stability.
Patella is held tightly against the knee joint, preventing anterior
displacement (Patella is not essential for knee stability).
b) Ligaments – Posterior Cruciate Ligament prevents femur sliding
forwards, so it’s the strongest ligament of the knee (to counter
direct effect of gravity). Anterior Cruciate ligament prevents femur
sliding backwards. Tibial & Fibular Collateral ligaments impart
lateral stability.
c) Muscles – Tone of Quadriceps extend the knee joint, opposed by
the tension of the hamstrings
5. Ankle – Countering the Tendency for Dorsiflexion

a) Bony – Trochlea of the Talus (which articulates with the Malleoli) is
wider anteriorly than posteriorly, so, when dorsiflexed, the Talus
is ‘stuck’ between the 2 malleoli, preventing further movement &
increasing stability in the dorsiflexed position.
b) Ligaments – Deltoid Ligament & lateral ligament impart lateral
stability
c) Muscular – Tendency for dorsiflexion countered by bulky
plantarflexors (Gastrocnemius, Soleus, Long flexors)
6. Sole – Refer Foot Arches

Neuro Science Final

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Neuro Science Final

Uploaded by

Copyright:

Available Formats

NEURO SCIENCE MODULE

1st MBBS Repeat Campaign - 2019

26TH BATCH – 2015/2016

Receive specific stimuli

Respond best to one form of energy

Convert external form of energy to recognizable energy

Sensory receptor stimulated

Change RMP Generator receptor potentials (GRP)

If GRP is similar or higher than threshold for stimulus

[Sensory transduction occurs through changes in membrane potentials]

Generator potentials Sensation

Non propagating action potentials: - Generator potentials occur

[Magnitude depend on intensity of stimulus ∴Graded potentials]

When the magnitude of the GP reaches a certain value, ab AP is produced

- Immediately contact with

Ex: Pain Interpretation of brain as,

↑ intensity of the sensations

- 128Hz tuning fork on finger tips/bones

B) Chronic pain (pathologic) : includes inflammatory and neuropathic pain

1.Slow pain, described as burning, throbbing pain – produced in tissue destruction

•Causalgia – a type of neuropathic pain

•HYPERALGESIA AND ALLODYNIA

Pain is often accompanied by

Hyperalgesia – an exaggerated response to a noxious stimulus

Hyperalgesia and allodynia indicate inceased sensitivity to nociceptive fibers.

Muscle Spindle – Consists of Intrafusal fibres

➢ Therefore, innervation by γ MNs increases Spindle Sensitivity of the

2) Clasp Knife Effect

Passive flexion of Elbow is attempted

When elbow is further flexed, Triceps is felt to be overstretched and GTO is

further flexion of elbow results in stretch of the relaxed Triceps

Above cycle of immediate resistance (Due to Stretch reflex)

Gives rise to a resembling movement of closing a pocket knife hence called as

➢ It is produced by damage to cell bodies in anterior gray column or its axon

UMN Lesions LMN Lesions

Spinal cord and tracts Nucleus Position Afferents

2.Posterior horn/gray column – sensory

• 4 nerve cell groups

3.Lateral gray horn Ascending Tracts (1) Lateral spinothalamic tract

• Thoracic and upper Lumbar segments only

Sternocleidomastoid and Forms lateral spinothalamic tract and ascends upwards

Unknown distribution Spinal lemniscus of Medulla Oblongata

Posterior limb of internal capsule

Sensory cortex of postcentral gyrus

(2) Anterior Spinothalamic tract (3) Dorsal column/Medial leminiscal pathway

Cell body in the dorsal root ganglion

Synapse with 2nd order neuron in substantia

Medial leminiscus at pons

Corona radiata Posterior limb of internal capsule

(4) Posterior spinocerebellar tract (5) Anterior spinocerebellar tract

Enters the posterolateral aspect of white column on the same side

Forms contralateral anterior Forms ipsilateral anterior

Inferior cerebellar peduncle Through medulla oblongata, Through medulla oblongata,

Ipsilateral cerebellar cortex (Doesn’t reach the cerebral cortex)

Contralateral cerebellar Ipsilateral cerebellar

Descending Tracts (1) Pyramidal Tracts/Corticospinal tracts Spinal cord injuries

80% decussate 20% no decussation

Forms and descends 1. Vasomotor changes

(Contralateral side) (ipsilateral side) •If the lesion is above T1

Decreased sympathetic effects on heart as sympathetic

Synapse with lower motor neurons

Decreased HR Bladder, voiding reflexes recover – automatic bladder.

No inhibition or facilitation from higher centers.

2. Autonomic changes Loss of sympathetic tone. Voiding