ICS Unit 3

1. Outer Ear (Sound Collection)

The outer ear collects sound waves and directs them toward the eardrum.

Main parts:

1. Auricle (Pinna): The visible ear that funnels sound into the ear canal.

2. Ear Canal: Also called the external auditory canal.
   It acts like a tube guiding sound waves to the eardrum.

Sound waves travel through the canal until they hit the eardrum.

2. Middle Ear (Sound Amplification)

The middle ear converts air vibrations into mechanical vibrations.

Eardrum (Tympanic Membrane)

When sound waves hit the eardrum, it vibrates.

Etymology

• tympanum (Greek) = drum

So it literally means “drum membrane.”

Ossicles

The three smallest bones in the body:

Bone	Meaning	Function
Malleus	hammer	attached to eardrum
Incus	anvil	connects bones
Stapes	stirrup	pushes into inner ear

These bones amplify vibrations about 20×.

B)

endolymph is in scala media; it has high K+

you missed a slide.

B)

This figure shows how hair cells in the inner ear convert mechanical movement (sound or head motion) into electrical signals. This process is called mechanotransduction.

Hair cells are located in the Cochlea and are responsible for detecting sound vibrations.

Let’s walk through the three panels from left to right.

1. Structure of the Hair Cell

At the top of the cell are stereocilia (hair-like projections).

Inside these stereocilia are mechanically gated ion channels.

Important ions involved:

• K⁺ (potassium) (very top)

• Ca²⁺ (calcium) (middle)

At the bottom of the hair cell is a synapse with a primary afferent neuron that carries signals to the brain through the Vestibulocochlear Nerve.

2. Panel A — Resting State

When the stereocilia are not bent (resting), the hair cell is at its baseline electrical state.

What happens:

1. Some mechanically gated channels are slightly open.

2. A small amount of K⁺ enters the cell.

3. The cell releases a baseline level of neurotransmitter.

Result: The afferent neuron fires spontaneous action potentials.

The graph below shows a moderate baseline firing rate.

3. Panel B — Depolarization (Excitation)

When stereocilia bend toward the tallest cilium, the channels open wider.

Steps:

1. Mechanically gated channels open

2. K⁺ flows into the hair cell

3. The cell depolarizes

4. Voltage-gated Ca²⁺ channels open

5. Ca²⁺ enters the cell

6. More neurotransmitter is released

Result: The afferent neuron fires more action potentials.

The graph shows a higher firing frequency.

This signals increased sound intensity or movement.

4. Panel C — Hyperpolarization (Inhibition)

If stereocilia bend away from the tallest cilium, the channels close.

Steps:

1. Mechanically gated channels close

2. K⁺ cannot enter

3. The cell hyperpolarizes

4. Ca²⁺ channels close

5. Less neurotransmitter is released

Result: The afferent neuron fires fewer action potentials.

The graph shows reduced firing.

5. Why Potassium Enters the Cell

This is unusual because normally K⁺ leaves cells.

In the inner ear, however:

1. the surrounding fluid (endolymph) has very high potassium concentration

2. So potassium flows into the hair cell, causing depolarization.

6. Key Idea of the Diagram

Hair cells convert mechanical bending → electrical signals.

This allows the brain to interpret:

• sound vibrations

• head movement

• balance

7. Simple Summary of the Three States

Stereocilia Movement	Cell Effect	Neuron Firing
Neutral	baseline depolarization	normal firing
Bend toward tall cilium	depolarization	increased firing
Bend away	hyperpolarization	decreased firing

Bending of hair-cell stereocilia opens or closes mechanically gated potassium channels, which changes neurotransmitter release and alters the firing rate of auditory neurons to encode sound or movement.

If you'd like, I can also show you the full cochlear sound-transduction pathway (basilar membrane → tectorial membrane → hair cells → spiral ganglion → auditory cortex), which connects this cellular diagram to how hearing actually works in the brain.

C)

Tonotopic organization of the basilar membrane because frequency (pitch) in the cochlea is primarily encoded by place coding—that is, where along the basilar membrane the sound vibration is strongest.

1. The Key Structure: Basilar Membrane

Inside the Cochlea is the Basilar Membrane.

Cochlea = “snail shell.”

The structure in the inner ear is named this because it looks like a spiral snail shell.

Hair cells sit on this basilar membrane.

When sound enters the cochlea, it creates traveling waves in the cochlear fluid, causing the basilar membrane to vibrate.

2. The Basilar Membrane Is Not Uniform

Different parts of the membrane respond to different sound frequencies.

Region of cochlea	Membrane properties	Frequency detected
Base (near oval window)	stiff and narrow	high frequencies
Apex (near helicotrema)	wide and flexible	low frequencies

This arrangement is called tonotopy.

3. What “Tonotopic Organization” Means

Etymology

• tono- = tone (sound frequency)

• -topic = place or location

So tonotopic organization = different frequencies are represented at different locations.

Each sound frequency peaks at a specific place along the basilar membrane.

Example:

• 16,000 Hz → base of cochlea

• 200 Hz → apex of cochlea

Hair cells at that location activate the Cochlear Nerve, telling the brain which frequency is present.

cochlea

C)

A)

B)

C)

A)

A)

A)

vestibular pathways

This diagram shows the vestibular pathways, which are the neural circuits that allow the brain to maintain balance, stabilize vision, and control posture when the head moves.

The signals begin in the inner ear balance organs and travel through brainstem nuclei to the eye muscles, spinal cord, and cerebellum.

1. Where the Signals Start (Vestibular Organs)

The movement of the head is detected in the Semicircular Canals, Utricle, and Saccule.

Functions

Structure	Detects
Semicircular canals	rotational head movement
Utricle	horizontal acceleration
Saccule	vertical acceleration

These signals travel through the Vestibular Nerve.

2. Vestibular Nuclei (Processing Centers)

The signals reach the vestibular nuclei in the brainstem.

Main nuclei:

Abbreviation	Name
SVN	superior vestibular nucleus
MVN	medial vestibular nucleus
LVN	lateral vestibular nucleus
IVN	inferior vestibular nucleus

These nuclei coordinate eye movement, posture, and balance.

3. Pathways From the Semicircular Canals

A. Eye Movement Control

Semicircular canals → SVN (superior vestibular nucleus, it is one of the four vestibular nuclei located in brainstem) → cranial nerves controlling eye muscles.

These include:

• Oculomotor Nerve

• Trochlear Nerve

• Abducens Nerve

This pathway stabilizes vision when the head moves.

It forms the vestibulo-ocular reflex (VOR).

Example:

When you turn your head right, your eyes automatically move left to keep your gaze stable.

B. Cerebellar Coordination

Semicircular canals → MVN → cerebellum

The Cerebellum uses this information to fine-tune balance and coordination.

C. Spinal Cord Control

Semicircular canals → MVN → spinal cord

These signals adjust neck muscles and posture

4. Pathways From the Utricle

Utricle → LVN → extensor motor neurons

This pathway forms the lateral vestibulospinal tract.

Function:

• activates extensor muscles

• maintains upright posture

Example:
When you lean forward, this reflex activates muscles to prevent you from falling

5. Pathways From the Saccule

Saccule → LVN → extensor motor neurons

Also contributes to postural reflexes.

Another pathway:

Saccule → IVN → cerebellum

This provides balance information for coordination.

6. The Medial Longitudinal Fasciculus (MLF)

In the diagram you see the Medial Longitudinal Fasciculus.

This tract connects:

• vestibular nuclei

• eye muscle nuclei (III, IV, VI)

It allows rapid coordination of eye movements with head movement.

7. Big Picture

Vestibular pathways have three major functions:

Function	Pathway
stabilize vision	vestibulo-ocular reflex
maintain posture	vestibulospinal tracts
coordinate balance	cerebellar connections

B)

D)

A)

she guarantees one of not multiple questions on this next exam.

A)

C)

COWS:

cold→ opposite

warm → same

B)

B)

jerking eye movement (tiny but still there)

Saccades

-can be voluntary and involuntary

-this is normal, however, neurological disorder represents delay, undershooting or overshooting.

superior colliculus are most involved in saccadic eye movements.

A)

B)

vergence and convergence

B)

general appearance

These terms come from neurology and physical examination, especially when evaluating movement disorders during a clinical exam.

very important

1. cerebral cortex excites the basal ganglia

2. basal ganglia sends inhibitory signals to the thalamus

3. thalamus excites the cerebral cortex

1. Step 1 — Cortex Excites the Basal Ganglia

The cerebral cortex sends excitatory signals (glutamate) to the striatum (caudate + putamen).

cerebral cortex (+) → Basal ganglia

Meaning: The cortex is basically saying: “I want to make a movement”

2. Step 2 — Basal Ganglia Inhibit the Thalamus

The output of the basal ganglia (mainly the globus pallidus interna) sends inhibitory signals (GABA) to the thalamus.

basal ganglia (-) → Thalamus

So normally the basal ganglia act like a brake on the thalamus.
basal ganglia = movement brake

3. Step 3 — Thalamus Excites the Cortex

The thalamus sends excitatory signals back to the cortex.

thalamus (+) → Cortex

When the thalamus is active, it stimulates the motor cortex, which then sends commands to the muscles.
4. Why This Loop Exists

The purpose of this loop is to control which movements are allowed.

The basal ganglia do two things:

1. Allow desired movements

2. Suppress competing movements

So they help make movements:

• smooth

• precise

• coordinated

5. The Important Concept: “Disinhibition”

Movement happens when the basal ganglia temporarily remove their inhibition of the thalamus.

Normal state:

Basal ganglia inhibit thalamus
↓
Movement suppressed

When movement is selected:

Basal ganglia reduce inhibition
↓
Thalamus activates cortex
↓
Movement occurs

This process is called disinhibition.

6. Simplified Analogy

Think of the system like a car.

Structure	Analogy
Cortex	driver
Basal ganglia	brake
Thalamus	accelerator
Muscles	wheels

So movement occurs when:

Brake released
↓
Accelerator pressed
↓
Car moves

1. Chorea Etymology

• Greek (choreia) = dance

• Root choros = dance or chorus

Chorea refers to irregular, unpredictable, dance-like movements.

The movements:

• are rapid

• non-rhythmic

• move randomly from one body part to another

It looks like the patient is dancing involuntarily.

Example diseases

• Huntington's disease

• Sydenham chorea

Mechanism

Usually due to damage to the basal ganglia, especially the striatum. why?

To understand why damage to the basal ganglia (especially the striatum) causes chorea, we need to look at how the basal ganglia normally control movement. The key idea is that the basal ganglia act as a movement filter:

• they allow desired movements

• they suppress unwanted movements

When that filtering system breaks, extra unwanted movements escape, which appear clinically as chorea.

1. What the Basal Ganglia Normally Do

The main structures involved are:

• striatum (caudate + putamen)

• globus pallidus

• subthalamic nucleus

• substantia nigra

• thalamus

The striatum is the input center of the basal ganglia.

It receives signals from:

• the cerebral cortex (motor plans)

• dopamine from the substantia nigra

The basal ganglia then regulate the motor cortex through the thalamus.

So the circuit is roughly:

cortex → striatum → globus pallidus → thalamus → cortex

The basal ganglia use two major pathways to regulate movement.

2. The Two Pathways That Control Movement Direct Pathway

Purpose: facilitates movement

Sequence:

1. cortex excites striatum

2. striatum inhibits GPi

3. GPi normally inhibits thalamus

4. Wen GPi is inhibited → thalamus becomes active

5. Thalamus excites motor cortex

6. movement occurs

So the direct pathway turns movement ON.

Indirect Pathway

Purpose: suppresses unwanted movement

Sequence:

1. cortex exicites striatum

2. striatum inhibits GPe

3. GPe normally inhibits subthalamic nucleus

4. When GPe is inhibited → subthalamic nucleus becomes active

5. Subthalamic nucleus excites GPi

6. GPi strongly inhibits thalamus

7. Movement is suppressed.

So the indirect pathway turns movement OFF.

3. What Happens in Chorea

In chorea (like in Huntington's disease), the first neurons that die are in the striatum, specifically:

GABA neurons of the indirect pathway

This produces the following effect.

Step-by-step

1⃣ Striatal neurons of the indirect pathway degenerate

2⃣ The globus pallidus externa (GPe) is no longer inhibited

3⃣ GPe becomes overactive

4⃣ GPe inhibits the subthalamic nucleus too strongly

5⃣ The subthalamic nucleus becomes underactive

6⃣ The globus pallidus interna (GPi) receives less excitation

7⃣ GPi fails to inhibit the thalamus

8⃣ The thalamus becomes overactive

9⃣ The thalamus overstimulates the motor cortex

🔟 The motor cortex produces excess, uncontrolled movements

These are the jerky, dance-like movements of chorea.

2. Athetosis Etymology

Greek (athetos)

• a- = without

• thetós = fixed or placed

Meaning “without a fixed position.”

Athetosis refers to slow, writhing, snake-like movements.

Characteristics:

• slow

• continuous

• twisting

• mostly affects hands and fingers

The fingers may look like they are slowly twisting or flowing.

Cause

Often seen in:

• cerebral palsy

• basal ganglia injury

Athetosis is a hyperkinetic movement disorder characterized by slow, continuous, writhing movements, usually of the hands, fingers, feet, or face. The cause almost always involves damage to parts of the basal ganglia, particularly the striatum, especially the putamen and globus pallidus.

1. Primary Cause: Basal Ganglia Injury

The most common cause of athetosis is damage to the basal ganglia, especially:

• Putamen

• Globus pallidus

• sometimes the caudate nucleus

These structures normally regulate muscle tone and suppress unwanted movements.

When they are damaged:

• inhibitory motor control is disrupted

• competing motor signals are not suppressed

• muscles receive irregular signals

This produces slow twisting movements.

4. Why Movements Are Slow (Unlike Chorea)

Movement disorders depend on which part of the basal ganglia is damaged.

Disorder	Movement type	Speed
Chorea	jerky dance-like movements	fast
Athetosis	twisting writhing movements	slow
Hemiballismus	violent flinging movements	very fast

Athetosis often involves globus pallidus dysfunction, which affects muscle tone regulation, producing sustained slow contractions.

4. Dystonia Etymology

Greek:

• dys- = abnormal or difficult

• tonos = tension or muscle tone

Meaning abnormal muscle tone.

Meaning

Dystonia = sustained muscle contractions that produce:

• twisting movements

• abnormal postures

Example:

• neck twisted to one side

• hand locked in abnormal position

Mechanism

Usually due to basal ganglia dysfunction.

Dystonia occurs when the basal ganglia fail to properly regulate muscle activation, causing sustained, involuntary contractions and abnormal postures. To understand why, we need to look at what the basal ganglia normally do in movement control.

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1. What the Basal Ganglia Normally Do

The basal ganglia function as a movement selection and inhibition system.

Their main job is to:

1. Select the desired movement

2. Suppress competing movements

3. Control muscle tone and posture

They do this through loops involving:

• Striatum (caudate + putamen)

• Globus pallidus interna (GPi)

• Globus pallidus externa (GPe)

• Subthalamic nucleus

• Thalamus

• Motor cortex

Normally: basal ganglia → regulate thalamus → regulate motor coordination

The GPi sends inhibitory signals to the thalamus, acting as a movement brake.

2. What Goes Wrong in Dystonia

In dystonia, basal ganglia inhibition becomes abnormal.

Specifically:

1. GPi output becomes irregular or reduced

2. The thalamus becomes overactive

3. The motor cortex receives excessive or disorganized signals

4. Multiple muscle groups activate simultaneously

Instead of one muscle contracting while the opposite relaxes:

agonist muscle contractions

antagonist muscle also contracts

This produces:

• twisting

• sustained contractions

• abnormal postures

3. Loss of “Surround Inhibition”

One key mechanism is the loss of surround inhibition.

Normally the basal ganglia do this:

-activate the desired movement

-suppress the surrounding muscles

Example:

To move your finger:

• finger flexor muscles activate

• neighboring muscles are inhibited

In dystonia: Finger flexor activated
Nearby muscles also activated

Result:

• twisting

• abnormal posture

4. Abnormal Muscle Co-Contraction

Because the inhibitory control is lost:

• agonist and antagonist muscles contract together

Example in cervical dystonia: sternocleidomastoid + opposing neck muscles both contract.

This produces torticollis (twisted neck).

5. Role of Dopamine and Neurotransmitters

Basal ganglia circuits depend on several neurotransmitters:

• dopamine

• GABA

• acetylcholine

Imbalance in these signals can disrupt motor control.

Examples:

• dopamine dysfunction

• abnormal GABA inhibition

• cholinergic imbalance

These disrupt the precision of motor control circuits.

6. Structural Areas Often Involved

The structures most associated with dystonia include:

• putamen

• globus pallidus interna

• thalamus

• cerebellar connections

Modern research shows dystonia involves a network disorder, not just a single nucleus.

5. Torticollis Etymology

Latin:

• tortus = twisted

• collum = neck

Meaning “twisted neck.”

A form of cervical dystonia where the neck muscles contract and the head turns to one side.

Torticollis (twisted neck) is most commonly a form of cervical dystonia, meaning the neck muscles contract involuntarily due to abnormal motor control circuits, particularly involving the basal ganglia and brainstem motor pathways. The mechanism can be understood at three levels: muscular, neural circuits, and neurotransmitters.

It describes a condition where the head is pulled to one side, rotated, or tilted due to involuntary muscle contraction.

2. Muscles Involved

The main muscle responsible is usually the:

• sternocleidomastoid (SCM)

Etymology

• sterno = sternum

• cleido = clavicle

• mastoid = mastoid process of temporal bone

Function of SCM:

Muscle contraction	Head movement
One SCM contracts	head rotates to opposite side
Both SCM contract	neck flexion

The most common cause of torticollis is basal ganglia dysfunction.

Normally the basal ganglia:

• coordinate muscle activity

• suppress unwanted movements

• ensure only the correct muscles activate

In cervical dystonia:

1. basal ganglia inhibition fails

2. Motor cortex sends EXCESSIVE signals

3. Neck muscles receive abnormal activation

4. Sustained Muscle contraction occurs

The globus pallidus interna (GPi) normally inhibits the thalamus.

If this inhibition becomes abnormal:

1. thalamus becomes overactive

2. motor cortex overstimulated

3. neck muscles contract involuntarily

In torticollis, one SCM contracts continuously, causing:

• head rotation

• head tilt

• abnormal posture

Other neck muscles may also be involved:

• splenius capitis

• trapezius

• levator scapulae

Causes

• congenital

• trauma

• neurological disorders

The head may appear:

• tilted

• rotated

• pulled to one side.

6. Opisthotonos Etymology

Greek:

• opistho- = behind

• tonos = tension

Meaning “backward muscle tension.”

A severe spasm where the body is arched backward.

Appearance:

• head and heels bent backward

• spine severely arched

Causes

Seen in severe neurological conditions like:

• Tetanus

• meningitis

• severe brain injury

Mechanism:

• extreme muscle hypercontraction.

3. Normal Motor Control

Normally, muscle tone is controlled by a balance between excitatory and inhibitory signals in the central nervous system.

Important inhibitory neurons use GABA and glycine.

These inhibitory signals suppress excessive muscle contraction.

Normal balance:

excitatory signals → activate muscles

inhibitory signals → limit contraction

4. What Goes Wrong in Opisthotonos

In opisthotonos, inhibitory control is lost.

This causes overactivation of motor neurons in the spinal cord.

Mechanism:

Loss of inhibitory interneurons
↓
Alpha motor neurons become hyperactive
↓
Extensor muscles contract continuously
↓
Severe body arching

5. Classic Cause: Tetanus

The most famous cause is infection by
Tetanus.

Mechanism in tetanus

The bacterium produces tetanospasmin toxin.

Step-by-step:

1. Toxin enters peripheral nerves

2. Travels retrograde along axons to the spinal cord

3. Blocks release of inhibitory neurotransmitters

Specifically blocks:

• GABA

• glycine

This occurs in Renshaw inhibitory interneurons.

Result:

No inhibition of motor neurons
↓
Continuous firing of motor neurons
↓
Severe muscle spasms
↓
Opisthotonos

6. Why Extensor Muscles Dominate

Extensor muscles (anti-gravity muscles) are normally more strongly activated in the spinal cord.

When inhibition disappears:

Extensors overpower flexors
↓
Body arches backward

This is why opisthotonos produces backward arching rather than forward bending.

7. Tardive Dyskinesia Etymology

Tardive

• Latin tardus = slow or delayed

Dyskinesia

• dys- = abnormal

• kinesis = movement (Greek kinesis = motion)

• 
  “Delayed abnormal movement.”

Meaning

A movement disorder caused by long-term dopamine receptor blockade.

Most commonly due to antipsychotic drugs.

Characteristic movements

• lip smacking

• chewing motions

• tongue protrusion

• teeth grinding

• facial grimacing

These movements are:

• repetitive

• involuntary

Mechanism

Chronic dopamine blockade causes dopamine receptor supersensitivity in the basal ganglia.

2. Brain Structures Involved

The disorder primarily affects the basal ganglia, especially:

• striatum (caudate + putamen)

• globus pallidus

• motor cortex circuits

The striatum is critical because it contains neurons with dopamine D₂ receptors that regulate movement.

3. Normal Dopamine Function in the Basal Ganglia

Dopamine from the substantia nigra modulates two pathways:

Direct pathway

Promotes movement.

Indirect pathway

Suppresses movement.

Dopamine:

• stimulates the direct pathway

• inhibits the indirect pathway

Net effect:

Dopamine → promotes smooth voluntary movement

4. What Antipsychotic Drugs Do

Many antipsychotic medications block dopamine D₂ receptors.

Examples include:

• Haloperidol

• Chlorpromazine

Mechanism:

Drug blocks dopamine receptors
↓
Dopamine signaling decreases
↓
Indirect pathway becomes dominant
↓
Movement suppression

Early on this can cause parkinsonian symptoms.

5. Long-Term Adaptation of the Brain

With chronic dopamine blockade, neurons adapt.

They do this by increasing the number and sensitivity of dopamine receptors.

This process is called dopamine receptor supersensitivity.

Mechanism:

Chronic D₂ blockade
↓
Neurons upregulate dopamine receptors
↓
Receptors become hypersensitive

6. When Dopamine Stimulates These Receptors

Once the receptors become hypersensitive:

Even small amounts of dopamine produce excessive motor activity.

Result:

Hypersensitive dopamine receptors
↓
Overactive striatal signaling
↓
Excess motor output
↓
Involuntary repetitive movements

These movements include:

• lip smacking

• chewing motions

• tongue protrusion

• teeth grinding

• facial grimacing

7. Why the Mouth and Face Are Commonly Affected

The orofacial region has strong representation in the basal ganglia motor circuits.

These circuits control:

• chewing

• swallowing

• speech movements

When dysregulated, they produce stereotyped oral movements.

8. Role of GABA and Other Neurotransmitters

Besides dopamine, other systems become abnormal:

• GABA neurons in the striatum degenerate

• cholinergic interneurons become imbalanced

• oxidative stress may damage neurons

These changes further destabilize motor control.

9. Why It Is “Tardive”

It is delayed because the receptor changes take months or years to develop.

Timeline:

Chronic dopamine blockade
↓
Gradual receptor upregulation
↓
Supersensitivity
↓
Dyskinesia appears

10. Summary of the Mechanism

The central mechanism is dopamine receptor supersensitivity in the basal ganglia.

Long-term D₂ receptor blockade
↓
Receptor upregulation
↓
Hypersensitive dopamine signaling
↓
Excess motor output
↓
Tardive dyskinesia

Resting Tremor

Resting: inactivity

Tremor: to shake

So resting tremor literally means “shaking that occurs when the body part is at rest.”

2. Definition

A resting tremor is a rhythmic shaking that appears when a muscle is relaxed and not actively being used.

Key characteristics:

• occurs when the limb is at rest

• decreases or disappears during voluntary movement

• often returns when movement stops

Example:

A patient’s hand shakes when resting in their lap but stops when they reach for an object.

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3. Classic Clinical Association

Resting tremor is most strongly associated with
Parkinson's disease.

Typical description:

“Pill-rolling tremor”

The thumb and fingers move as if rolling a pill or small object.

Frequency:

• about 4–6 Hz

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4. Brain Structures Involved

Resting tremor arises from dysfunction of the basal ganglia motor circuits.

Important structures include:

• substantia nigra pars compacta

• striatum (caudate + putamen)

• globus pallidus

• thalamus

• motor cortex

The critical structure is the substantia nigra, which produces dopamine.

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5. Normal Dopamine Function

The substantia nigra sends dopamine to the striatum through the nigrostriatal pathway.

Dopamine regulates two pathways:

Direct pathway

Facilitates movement.

Indirect pathway

Suppresses movement.

Dopamine normally:

• stimulates the direct pathway

• inhibits the indirect pathway

This produces smooth controlled movement.

6. What Happens in Resting Tremor

In Parkinsonian tremor:

• dopamine-producing neurons in the substantia nigra degenerate

Result:

Dopamine levels fall
↓
Indirect pathway becomes overactive
↓
Thalamus is excessively inhibited
↓
Motor signals become unstable

This instability produces oscillatory signals in motor circuits.
7. Oscillatory Circuit Formation

The tremor arises from rhythmic activity in a loop involving:

Basal ganglia
↓
Thalamus
↓
Motor cortex
↓
Muscles

Because dopamine regulation is lost, the circuit becomes unstable and oscillates rhythmically, producing tremor.

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8. Why Tremor Appears at Rest

During voluntary movement, the motor cortex and cerebellum strongly activate movement pathways, which temporarily suppress the abnormal oscillations.

When the limb is relaxed:

Basal ganglia oscillations dominate
↓
Tremor appears

This is why the tremor is called resting tremor.

9. Why the Hands Are Commonly Affected

The basal ganglia have strong representation for fine motor control of the hands and fingers.

Because these circuits are highly active, they are particularly sensitive to dopamine imbalance.

Thus tremor is often seen in:

• hands

• fingers

• jaw

• lips
  
  10. Summary of the Mechanism

Resting tremor occurs due to dopamine deficiency in basal ganglia circuits.

Mechanism:

Degeneration of substantia nigra neurons
↓
Reduced dopamine in striatum
↓
Basal ganglia circuit imbalance
↓
Rhythmic oscillatory activity
↓
Resting tremor

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✅ Key Concept

Resting tremor results from dopamine loss in the basal ganglia, which destabilizes motor control circuits and produces rhythmic oscillations that appear when the muscles are at rest.

Action Tremor 1. Etymology

Action

• Latin actio = a doing, performing, or movement

Tremor

• Latin tremere = to shake or quiver

So action tremor literally means “shaking that occurs during movement.”

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2. Definition

Action tremor is a tremor that occurs when a muscle is voluntarily activated, such as when:

• holding the arms out

• writing

• reaching for an object

• drinking from a cup

It appears during movement and usually disappears at rest.

This contrasts with resting tremor, which occurs when the muscle is relaxed.

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3. Main Brain Structures Involved

Action tremor is usually caused by dysfunction in the cerebellum or cerebellar circuits.

Important structures include:

• cerebellum

• dentate nucleus

• red nucleus

• thalamus

• motor cortex

These structures form the cerebellar motor coordination loop.

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4. Normal Cerebellar Function

The cerebellum acts as the brain’s movement coordinator.

It compares:

1. intended movement (from the motor cortex)

2. actual movement (from sensory feedback)

It then sends corrections to smooth the motion.

Normal circuit:

Motor cortex → movement command
↓
Cerebellum monitors movement
↓
Cerebellum corrects errors
↓
Smooth coordinated motion

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5. What Goes Wrong in Action Tremor

When the cerebellum or its output pathways are damaged, the brain cannot properly fine-tune movements.

This leads to oscillating corrections.

Mechanism:

Movement begins
↓
Error detected
↓
Correction overshoots
↓
Opposite correction occurs
↓
Repeated oscillation

This oscillation produces rhythmic shaking during movement.

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6. Types of Action Tremor

Action tremor includes several subtypes.
Postural tremor

Occurs when maintaining a position against gravity.

Example:
holding arms outstretched.

Common in
Essential tremor.

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Kinetic tremor

Occurs during voluntary movement.

Example:
writing or drinking.

---

Intention tremor

Occurs when approaching a target.

Example:
finger-to-nose test.

The tremor gets worse near the target.

Typical cause:

• cerebellar lesions

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7. Classic Cause: Essential Tremor

The most common cause of action tremor is
Essential tremor.

Features:

• postural and kinetic tremor

• hands and arms most affected

• improves with alcohol

• often familiar

It likely involves abnormal oscillations in the cerebellothalamic circuit.

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8. Other Causes

Action tremor may also occur in:

• cerebellar stroke

• multiple sclerosis

• brain tumors

• alcohol withdrawal

• hyperthyroidism

• medication side effects

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9. Why the Tremor Is Rhythmic

The tremor becomes rhythmic because motor control circuits form feedback loops.

If the cerebellar correction system is unstable:

Movement error
↓
Overcorrection
↓
Opposite error
↓
Repeated oscillation

This creates a regular shaking pattern.

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10. Summary

Action tremor mechanism

1. Voluntary movement begins

2. Cerebellar coordination system is impaired

3. Movement corrections overshoot

4. Oscillating corrections occur

5. Rhythmic tremor appears during movement

this will be the written portion of the exam.

reflexes

-this will be on your quiz.

memorize.

mental status

1. Orientation: examiner may ask the patients full name, the date (including the year), and the place in which he is being examined.

2. serial 7s: the examiner will ask the patient to subtract 7s from 100 in serial fashion as fast as he can (100, 93, 86, 79, etc.)

3. short term memory: by giving the patient three items to recall (eg. automobile, oven, book).

4. past memory: by asking historical questions like the name of the president and vice president, the governor of the state, the names of the last presidents, or current events

5. abstract reasoning: the examiner may ask the patient to tell him what is generally meant by several proverbs Examples: “Don’t count your children’s chickens before they’ve hatched".” “A stitch in time saves nine”, “People who live in glass houses shouldn’t throw bricks”.

cerebellar function

1. UE asks the patient to repeat alternating movements of the hand over the thigh on both sides

2. LE asks the patient to tap the examiners hand with the ball of each foot alternating

3. Finger to nose bilaterally: asks the patient to touch the index finger and then his nose (upper arm abducted)

4. Heel to shin bilaterally: asks the patient to place one heel on the opposite knee and then run it down the shin.

cranial nerves

1. test nerve II: (usually done with eye exam): vision, visual fields, Opthalmoscope

2. test nerve III, IV, VI: (usually done with eye exam): extraocular movements, pupillary reaction

3. test nerve VII: motor function: ask patient to: raise eyebrows, frown, close eyelids tightly (upper division)

4. (still nerve VII) show teeth, puff out cheeks, or smile (lower division)

5. test nerve IX and X: have the patient say “AH” and observe for midline elevation of the palate

6. test nerve XII: protrude the tongue, check for midline protrusion.

distal strength

1. assess for pronator drift- with extended arms out in front at shoulder level and palms facing upward, asks patient to close eyes, observes for drift

2. assess for distal strength: ask patient to walk on toes, heels, and stand on each tippy toe

3. observe gait (normal): asks patient to walk across the room

4. observes tandem gait: ask patient to wall heel -to-toe in a straight line

5. Romberg test: asks patient to first stand with feet together, close eyes with 20-30 secs without support.

romberg test for distal strength

amygdala has to do with fears, especially learned responses to fears.

hallucination: parahippocampal uncus

amygdala: fear, lesion in amygdala results in loss of fear

why is parahippocampal uncus the correct answer?

This question is describing olfactory hallucinations (also called phantosmia) that are:

• sudden

• brief

• episodic

This is classic for temporal lobe (uncinate) seizures.

Parahippocampal Uncus Definition

The uncus is the medial, anterior part of the parahippocampal gyrus in the temporal lobe, and it contains part of the primary olfactory cortex (piriform cortex + amygdala connections).

• Uncus = Latin for “hook”
  → hook-shaped structure

C)

A) and B)

B)

A)

A)

on the next exam, she will show you an image of the retina cells.

D)

D)

A)

B is correct.

ignore, C D and E because those are also not true.

E)

C)

SHE WILL ASK YOU ABOUT LESIONS IN ANYONE OF THESE DIFFERENT REGIONS.

LESIONS WILL GIVE YOU A VERY SPECIFIC DEFICIT IN THIS VISUAL FIELD.

B)

C)

D)

C)

A)

E)

A)

it’s in the book.

E)

C)

C)

B)

B)

C)

C)

B)

D)

C)

B)

C)

C)

B)

B)

A)

C)

B)

A)

C)

I think you missed a question.

C)

B)

B)