Exam 1: Palpebral Closure and Tears

Eyelid functions (5)

Globe protection, produce tear film, spread tear film, assist in tear drainage, provide O2 to tear film (closed eye)

Muscles of palpebrae (5)

Orbicularis occuli, horner’s, riolan’s, levator, Muller’s

Skeletal palpebrae muscles

Orbicularis occuli, Horner’s, Riolan’s, Levator

Smooth palpebrae muscles

Muller’s

Orbicularis occuli innervation

CN VII

Levator innervation

CN III

Horner’s innervation

CN VII

Riolan’s innervation

CN VII

Muller’s innervation

Sympathetic

Horner’s function

Squeezes canaliculi

Riolan’s function

Holds lid close to globe, squeezes meibomian glands

Muller’s function

Additional lid elevation

Fasciculus

A group of fibers (cells) in skeletal muscle

Fiber

A cell in skeletal muscle

Sarcomere

Intracellular molecular structure in skeletal muscle

Actin

Polymeric molecule made of fibers in a sarcomere

Myosin

Motor function in sarcomere

How does skeletal muscle contract?

Myosin head associates with F-actin > Release ADP which induces myosin head movement and power stroke > myosin head attaches to ATP and releases F-actin > ATP is hydrolyzed to ADP causing the myosin head to bend back and store potential energy

Type I fibers also called

Slow twitch or slow oxidative

Type IIA fibers also called

Fast twitch or fast oxidative

Type IIX fibers also called

Fast twitch or fast glycotic

Muscle fiber types in order from slowest to fastest

I, IIa, IIx

What determines rate of muscle fiber reaction?

Speed of myosin ATPase activity (ATPase hydrolysis step)

How do type I fibers make energy?

Aerobic respiration

How do type IIA fibers make energy?

Mostly aerobic respiration, but can switch to anaerobic glycolysis

How do type IIX fibers make energy?

Anaerobic glycolysis

Which muscle fibers have the highest capillary density? Why?

Type I, because they need O2 from blood for aerobic respiration

Which muscle fibers fatigue the fastest and slowest? Why?

Type IIX fatigues the fastest and I the slowest because IIX uses anaerobic glycolysis and I uses aerobic respiration

Which muscle fibers have the most mitochondria? Why?

Type I, because they need to work over longer periods of time (need more energy production, high aerobic respiration)

What type of muscle fibers are in the orbicularis occuli? Why?

I and II but mostly II, because II is used for rapid closure

What type of muscle fibers are in the levator? Why?

I and II but mostly II, because II is used for lid elevation during a blink

Neurotransmitter

Small molecule released by neurons to stimulate the function of the receiving cell

Acetylcholine

Neurotransmitter that stimulates skeletal muscle cells

Synaptic vesicle

Membrane-bound intracellular structure containing neurotransmitters

How does muscle contraction work in regards to the neuromuscular junction?

Ach is secreted from nerves and binds to AChR on muscle cell > ion channels open > generate AP in muscle cell and t tubules > SR is triggered to release calcium > Ca binds troponin and causes it to dissociate from F actin > without troponin, myosin can bind to actin and contract the sarcomere

Diplopia

Double vision

Peek sign

Ocular surface uncovered following sustained closure (can’t keep eyes fully closed for extended periods of time)

What muscles of the eyelid are fast-twitch?

Orbicularis occuli, levator (and extraocular muscles)

Diplopia, peek sign, and ptosis may all be caused by what common pathology?

Impaired function of neuromuscular junction (autoimmune)

Ocular myasthenia gravis

Autoimmune neuromuscular junction disorder of that affects some ocular muscles

What muscles are more susceptible to impaired neuromuscular junction?

Muscles with a lot of Type II fibers so levator, orbicularis, and extraocular muscles

What commonly causes impaired neuromuscular junctions?

Antibodies to Ach receptors of muscle cells—they block Ach and prevent the receiving muscle cell from propagating the signal

Why are fast twitch muscles more susceptible to disruption of neuromuscular junction function?

Because they require repeated nervous stimulation

How is ocular myasthenia gravis related to general MG?

2/3 of patients with OMG will develop GMG in 2 years

General myasthenia gravis

Systemic muscle weakness, difficulty swallowing (dysphagia), slurred speech

Who is more likely to suffer from ocular myasthenia gravis?

Males age 60-80 and females age 20-30 AND 60-80

Tarsal muscles innervation

Sympathetic

How does smooth muscle contract?

Calcium influx > triggers calcium released from sarcoplasmic reticulum > Ca binds calmodulin > Ca-CaM activates myosin light chain kinase (MLCK) > MLCK activates myosin > myosin contracts and pulls on actin

Horner’s syndrome presents as…

Ptosis, miosis, facial anhidrosis

What causes Horner’s syndrome?

Preganglionic/superior cervical ganglion lesion

Miosis

Pupil constriction d/t dilator muscle inhibition

Facial anhidrosis

Lack of sweating on the face

Ocular myasthenia gravis presentation

Ptosis, diplopia, peek sign

Palpebral motions (4)

Voluntary closure, spontaneous blink, reflexive blink, coordination with EOMs

Nasal angle during blink

Remains immobile

Temporal angle during blink

Moves nasally and downward

Upper lid during blink

Moves down and medially

Lower lid during blink

Moves mostly medially

Blink mechanism (superior palpebrae)

Baseline levator motor neuron firing ceases > LPS muscles relax > passive downward force of Whitnall’s ligament/canthal tendons lowers superior palpebrae > OO neuron firing begins causing further closure > OO neuron stops firing and muscle activity ceases > LPS motor neurons resume firing, reopening the palpebral aperature

Why close faster than opening?

Opening requires LPS to contract against passive downward forces where during closure the OO contracts unopposed and is assisted by passive downward forces. The OO also has more fast twitch fibers

Which part of the lid is like a stretched spring ready to snap closed?

Whitnall/Canthal tendons

Causes of increased blink rate

Decreased humidity, contact lens use, older age, speaking, heightened emotional states, and birth control

Causes of decreased blink rate

Increased humidity, younger age, sustained visual tracking, reading, daydreaming, downward gaze

Dopamine relationship to spontaneous blink rate (SBR)

Stimulation of dopaminergic nerves increases SBR

Spontaneous blink

“Normal” blinking

Parkinson’s relationship to SBR

Parkinson’s decreases dopamine > decreased SBR

Schizophrenia’s relationship to SBR

Schizophrenia increases dopamine > increased SBR

How does globe move during a blink?

Typically rotates inferiorly and medially but can be in a different direction depending on gaze

Saccade

Rapid simultaneous movement of both eyes in the same direction from one point of fixation to another

Saccades controlled by…

Frontal eye fields and superior colliculus

Bell’s Phenomenon

A reflex in which the eyes are seen to roll up and out (abduct) when both eyelids are forcibly closed

During eye movement, superior rectus coordinates with…

Levator (both innervated by CN III)

During eye movement, inferior rectus coordinates with…

Inferior tarsal muscles

Ptosis by oculomotor nerve palsy

CN III palsy > Levator and EOMs (IR, SR, MR, IO) fail to function resulting in inability to look up, down, or medially > resting eye position down and out d/t continued functioning of SO and LR

Aponeurotic ptosis

Disruption of the levator/aponeurosis insertion

Mechanical ptosis

Can be caused by tumor or palpebral inflammation

Dermatochalasis

Sagging skin covers eye (not ptosis)

Marcus Gunn Jaw Winking Phenomenon

Pterygoid muscle (CN V) linked to levator (CN III) at cortical level; results in ptosis at rest and LPS activation upon jaw motion

Benign essential blepharospasm

Idiopathic, begins with elevated blink rate that progressively increases

Benign essential blepharospasm cause

Trigeminal reflex blink hyperexcitability and contraction of OO

Myokymia

Eye twitching caused by a small hyperexcitability of portion of the muscle fibers of the OO

Blepharospasm treatment

Botulism toxin (Botox) interferes with synaptic vesicles

Botulism toxin produced by

Clostridium botulinum and related bacteria

Lid-opening apraxia

Inability to initiate and sustain eyelid opening, typically observed with blepharospasms

Lid-opening apraxia cause

Involuntary inhibition of LPS activity or contraction of the pretarsal portion of the OO

Bell’s Palsy can result in what lid disorder

Lagophthalmos, due to facial weakness caused by CN VII lesion

TED causes

Autoimmune: immune cells stimulate the TSH receptor

TED risk factors

Women 5-6x more likely than men; smoking

Dalrymple’s Sign

Retraction of the upper lid

Von Graefe’s Sign

Upper lid lag on downward gaze

TED complications (vision threats)

Exposure keratopathyand compressive optic neuropathy

Pseudo-Graefe Phenomenon

Fibers intended to go to the medial rectus get misdirected to the levator instead following recovery from CN III paralysis

Pseudo-Graefe’s Sign

Lid retraction in downward inward gaze