Cranial Nerves Flashcards
What are the 12 cranial nerves?
Olfactory, Optic, Oculomotor, Trochlear, Trigeminal, Abducens, Facial, Vestibulo-cochlear, Glossopharyngeal, Vagus, Accessory, Hypoglossal.
Fundus examination?
By causing the dilation of the pupil pharmacologically, the physician can examine the fundus through the ophthalmoscope.
The optic nerve head (optic disk) can be easily identified by the radially emerging blood vessels originating in the center of the optic nerve. It is the area in which all the fibers converge to create the optic nerve.
The fovea forms the center of the retina and is surrounded by the macula (fovea and macula can be identified by the relative absence of large diameter blood vessels).
Types of visual abnormalities ?
Pupillary reflex physiology and abnormalities : The pupillary reflex involves direct and consensual pupil constriction (miosis) when light is directed toward the eye. It is controlled by two pathways —> Parasympathetic pathway (sphincter pupillae) and the sympathetic pathway (dilator pupillae). An abnormality is ANISOCORIA or unequal pupil size due to parasympathetic deficits (e.g., III nerve palsy or Adie’s pupil) in bright light or sympathetic deficits (e.g., Horner’s syndrome) in dim light.
Optic nerve lesions : lesions based on location such as
- prechiasmal lesions : monocular vision loss due to complete nerve lesion, concentric visual field constriction and central scotoma.
- chiasmal lesions : bitemporal heteronymous hemianopsia and junctional field defect.
- post chiasmal lesions : homonymous hemianopsia, superior and inferior quadrantanopia and altitudinal hemianopsia.
Specific disorders include optic neuritis, papilledema, central retinal artery occlusion, Horner syndrome and infectious disorders.
Disorders of eye movements : main causes are muscle diseases or neuromuscular junction issues, lesions at nerve or isolated causes like trauma and ischemic lesions.
- strabismus : horizontal can be exotropia (outward) or esotropia. Vertical can be hypertropia (higher eye) or hypertropia.
Isolated nerve palsies :
- CNIII ptosis, fixed dilated pupil caused by compression or ischemia.
- CN IV vertical diplopia and head tilt.
- CN VI horizontal diplopia and inward eye deviation.
Complex syndromes include internuclear opthalmoplegia, horizontal gaze palsy and one and a half syndrome.
Trigeminal nerve anatomy?
The trigeminal nerve is the largest cranial nerve and has both sensory and motor components. It originates from the pons and contains a large sensory root and a smaller motor root. The trigeminal (Gasserian) ganglion, located in Meckel’s cave, contains the cell bodies of sensory neurons. The nerve divides into three branches: ophthalmic (V1), maxillary (V2), and mandibular (V3).
- Sensory Components
The sensory root carries information from the face, scalp, cornea, nasal cavity, oral cavity, meninges, and teeth. Sensory fibers synapse in the three trigeminal nuclei in the brainstem:
1. Principal Sensory Nucleus (Pons) – Fine touch and proprioception.
2. Spinal Nucleus (Extends to C3) – Pain and temperature sensation.
3. Mesencephalic Nucleus (Midbrain) – Jaw proprioception (jaw jerk reflex).
- Motor Components
The motor nucleus of CN V is located in the pons and provides bilateral corticobulbar innervation. The motor fibers bypass the trigeminal ganglion and travel within V3 (mandibular nerve) to innervate the muscles of mastication (masseter, temporalis, pterygoids), mylohyoid, anterior digastric, tensor tympani, and tensor veli palatini.
Branches of CN V
1. Ophthalmic (V1) – Sensory
• Exits via the superior orbital fissure.
• Innervates the forehead, scalp, upper eyelid, cornea, nasal bridge, and meninges.
2. Maxillary (V2) – Sensory
• Exits via the foramen rotundum.
• Innervates the lower eyelid, upper lip, cheek, upper teeth, nasal cavity, maxillary sinus, and meninges.
3. Mandibular (V3) – Sensory & Motor
• Exits via the foramen ovale.
• Sensory: Lower lip, chin, jaw, lower teeth, anterior 2/3 of the tongue (somatic sensation, not taste).
• Motor: Muscles of mastication, tensor tympani (ear), tensor veli palatini (soft palate movement).
Examination of the trigeminal nerve?
- Sensory Examination
• Assess all three divisions (V1: ophthalmic, V2: maxillary, V3: mandibular) bilaterally.
• Test light touch, pinprick, and temperature sensation on the face.
• Corneal reflex (tests V1 and V2 as afferent pathways, CN VII as efferent): Stimulate the cornea with cotton or air. A normal response includes eye closure and tearing. Absence suggests a lesion in V1 (afferent) or CN VII (efferent).
• Electrophysiological tests can assess nerve conduction and reflex latency. - Motor Examination
• Mastication muscles (masseter, temporalis, pterygoids): Ask the patient to clench the jaw while palpating the muscles.
• Check for weakness, atrophy, or fasciculations.
• Test jaw opening and lateral deviation against resistance. - Jaw Jerk Reflex
• Afferent: V3 proprioceptive fibers.
• Efferent: V3 motor fibers.
Procedure:
• Patient slightly opens the mouth, tap the chin with a reflex hammer. A normal response is minimal movement. An exaggerated reflex suggests bilateral upper motor neuron (UMN) lesions (e.g., pseudobulbar palsy, stroke, or motor neuron disease).
Causes of facial pain?
• Trigeminal neuralgia (tic douloureux): One of the most common and most challenging. The pain is really strong.
• Herpes Zoster: reactivation of the virus on your face or cornea.
• Postherpetic neuralgia
• Dental diseases (abscess): painful conditions, there is the formation of inflammation that leads to compression; therefore the pain fibers can be activated.
• Sinusitis: inflammation of the sinuses, it can be associated with headache.
• Ocular diseases (glaucoma): intraocular hypertension.
• Atypical facial pain (depressive syndromes): more challenging to be diagnosed.
• Cluster headache.
What is trigeminal neuralgia? Clinical features? Triggers?
Epidemiology : It is the most common cause of facial pain. Prevalence: 4 per 100,000 per year.
• More common in women than men.
• Typical onset in 6th and 7th decades.
• Younger patients may have symptomatic TN linked to Multiple Sclerosis (MS) or neoplasia.
• Risk factors: Age, hypertension, diabetes
Pain Characteristics
• Excruciating, lancinating, paroxysmal pain that is shooting, stabbing, electric shock-like.
• Paroxysms last a few seconds to less than a minute (rarely up to a few minutes).
• Unilateral in 97% of cases, bilateral in only 3% (suggestive of MS or brainstem pathology).
• Pain-free intervals occur initially but shorten over time.
• Episodes occur in bouts and can increase in frequency over time.
Affected Divisions of the Trigeminal Nerve
• Mandibular (V3) → most commonly affected.
• Maxillary (V2) → second most common.
• Ophthalmic (V1) → only 5% of cases.
Triggers :
Spontaneous or provoked by:
• Light touch (shaving, washing face).
• Chewing, talking, swallowing.
• Temperature changes (cold wind, drinking cold liquids).
• Severe weight loss in some patients due to avoiding eating.
Trigeminal neuralgia disease course? Pathogenesis?
Disease Course
• Early stages: Spontaneous remissions for weeks or months.
• Later stages: Bouts become more frequent, severe, and widespread.
• Pain spreads to wider areas of the face over time.
Pathogenesis
Primary (Idiopathic) TN
• Most cases are due to chronic vascular compression of the trigeminal nerve root at the dorsal root entry zone.
• Superior cerebellar artery is the most common culprit.
• Hypertension may worsen nerve damage over time.
Mechanism of Pain
1. Chronic pulsatile compression leads to focal demyelination of the nerve.
2. Ephaptic transmission: abnormal cross-talk between demyelinated trigeminal fibers leads to increased excitability.
3. Trigeminal-brainstem complex becomes hyperactive, amplifying pain perception.
Secondary TN
Structural lesions affecting the trigeminal system, such as:
• Brainstem tumors (pontine gliomas, MS plaques).
• Ponto-cerebellar angle lesions (acoustic neuroma, meningioma, aneurysm).
• Cavernomas, arteriovenous malformations.
DDX of trigeminal neuralgia?
Differential Diagnosis
• Secondary TN (due to compression, tumors, MS, etc.).
• Cavernomas: Can be seen on MRI T1 as an irregular hyperintensity with hemorrhagic leakage.
Other causes of facial pain:
• Dental disease, acute glaucoma, sinusitis, giant cell arteritis, angina (referred jaw pain).
• SUNCT (Short-lasting Unilateral Neuralgiform Headache with Conjunctival Injection and Tearing):
• Attacks last 1-5 minutes (longer than TN).
• Autonomic symptoms (lacrimation, rhinorrhea, conjunctival injection).
Treatment for trigeminal neuralgia?
Treatment
First-Line: Medical Therapy
1. Carbamazepine (400-800 mg/day)
• Most effective drug (sodium channel blocker).
• Side effects: Liver toxicity, sedation—monitor liver function.
2. Oxcarbazepine (900-1500 mg/day)
• Similar efficacy to carbamazepine but better tolerated.
3. Other options:
• Gabapentin (900–3600 mg/day) (used for refractory cases).
• Baclofen (40–80 mg/day) (myorelaxant, used in MS-related TN).
In cases of drug resistant TN :
1. Microvascular Decompression (MVD)
• Definitive treatment: removes vascular compression by placing a Teflon cushion.
• 90% success rate but invasive (intracranial surgery).
• Risks: Cranial nerve injury, CSF leaks.
2. Gasserian Ganglion Ablation
• Percutaneous procedure via foramen ovale.
• Radiofrequency thermocoagulation, glycerol, or balloon microcompression.
• Quick pain relief, but causes facial numbness.
3. Gamma Knife Radiosurgery
• Non-invasive focused radiation at the trigeminal nerve root.
• Delayed response (months) but effective for many patients.
Facial nerve anatomy?
The facial nerve (CN VII) is a mixed nerve responsible for motor, sensory, and autonomic functions. It originates in the pons, where the facial nucleus gives rise to motor fibers that wrap around the abducens nucleus (CN VI) before exiting the brainstem at the cerebellopontine angle. The nerve then travels through the internal acoustic meatus alongside CN VIII (vestibulocochlear nerve) before passing through the facial canal. Within the facial canal, intracranial branches arise, including the greater petrosal nerve, which carries parasympathetic fibers to the lacrimal gland, the chorda tympani, which conveys taste sensation from the anterior two-thirds of the tongue and parasympathetic innervation to the submandibular and sublingual glands, and the stapedial nerve, which controls the stapedius muscle to prevent hyperacusis. The nerve then exits the skull via the stylomastoid foramen, giving rise to extracranial branches that innervate the muscles of facial expression. These five major motor branches : temporal, zygomatic, buccal, marginal mandibular, and cervical—control different facial muscles, while the posterior auricular nerve supplies scalp muscles and carries sensory fibers.
Central supranuclear CN VII palsy?
A central CN VII palsy results from a lesion affecting upper motor neurons (e.g., stroke, tumor) before they reach the facial nucleus in the pons. Since the upper face receives bilateral cortical input, it remains unaffected, while the contralateral lower face is weak or paralyzed. Central facial palsy is often associated with ipsilateral limb weakness due to involvement of the corticospinal tract. It is commonly caused by stroke but can also be seen in progressive supranuclear palsy, where patients may experience apraxia of eyelid opening despite normal facial muscle strength.
Peripheral CN VII palsy? Causes?
A peripheral CN VII palsy occurs when the lesion affects the facial nerve after it exits the brainstem. It results in complete ipsilateral facial paralysis, involving both the upper and lower face. Depending on the lesion site, different clinical signs may be present:
1. Intracranial Lesion (proximal to the stylomastoid foramen)
• Motor paralysis of the entire ipsilateral face
• Lacrimal and salivary gland dysfunction (dry eye, dry mouth)
• Ageusia (loss of taste) in the anterior two-thirds of the tongue
• Hyperacusis (due to stapedius muscle paralysis)
2. Intracanalicular Lesion (after the stylomastoid foramen)
• Pure motor paralysis of the ipsilateral face
• No autonomic dysfunction or taste loss
• Possible sensory impairment of the external auditory canal
Causes of Peripheral CN VII Palsy
• Idiopathic (Bell’s Palsy) – often linked to viral reactivation (HSV-1, VZV), inflammation, or cold exposure.
• Herpes Zoster (Ramsay-Hunt Syndrome) – facial paralysis + painful vesicles in the ear.
• Compressive lesions – cholesteatoma, acoustic neuroma, carotid aneurysm, or temporal bone fracture.
• Meningitis (acute or chronic) – can affect the facial nerve intracranially.
• Autoimmune/Granulomatous Diseases – sarcoidosis, Guillain-Barré Syndrome (bilateral facial palsy), Lyme disease (bilateral palsy).
Key difference between central and peripheral CN VII palsy?
• Central CN VII Palsy = Contralateral lower face paralysis, forehead spared.
• Peripheral CN VII Palsy = Complete ipsilateral facial paralysis, including forehead.
What is Bell’s palsy?
Bell’s palsy is the most common peripheral CN VII palsy, also known as idiopathic peripheral facial nerve palsy, with an incidence of 20-25 per 100,000 per year. It results from inflammation and swelling of the facial nerve within the facial canal or at the geniculate ganglion, leading to nerve compression, ischemia, and demyelination. While the exact cause remains idiopathic, it is often associated with HSV-1 reactivation in younger individuals and vascular pathologies (diabetes, hypertension) in older adults. The onset is sudden (within hours) and worsens over 1-5 days, followed by gradual recovery over 2-4 weeks, with most patients showing complete or near-complete recovery within 1-3 months (75% cases). However, in severe cases, particularly when the intracanalicular portion is affected, permanent deficits may occur.
Clinical manifestation, diagnosis and treatment of Bell’s palsy?
Clinical Manifestations
• Facial asymmetry and weakness, with drooping of the mouth corner and inability to close the affected eye.
• Forehead involvement (distinguishing peripheral from central CN VII palsy).
• Corneal exposure due to lack of blinking → risk of corneal ulcers.
• Retroauricular pain (50% of cases).
Additional features (based on lesion site):
• Hyperacusis (stapedius muscle paralysis).
• Ageusia (loss of taste in anterior 2/3 of the tongue).
• Hypolacrimation (lesion before the greater petrosal nerve).
• Hyperlacrimation (“crocodile tears”) due to aberrant parasympathetic reinnervation.
Diagnosis is a clinical one, confirmed by exclusion of other causes:
• EMG (3-20 days after onset) assesses nerve degeneration severity.
• MRI is rarely needed but helps rule out MS or compressive lesions.
• CSF analysis is not routinely performed unless infection (meningitis) is suspected.
Treatment
• Eye protection: Artificial tears, eye patching, and lubrication to prevent corneal damage.
• Corticosteroids (1-2 mg/kg/day, tapered over weeks): Most effective when started within 72 hours to reduce inflammation and nerve compression.
• Antivirals (Acyclovir, 400-800 mg/day): Controversial, but considered if HSV involvement is suspected.
Complications of Bell’s palsy?
Complications & Sequelae
• Aberrant facial reinnervation → Synkinesis (involuntary muscle contractions during voluntary movements, e.g., involuntary eye closure with mouth movements).
• Misguided autonomic reinnervation → “Crocodile tears” (excessive lacrimation while eating).
• Hemifacial spasm: Persistent, benign facial twitching due to nerve hyperactivity.
What is hemifacial spasm? Causes?
Hemifacial spasm is a condition characterized by unilateral, involuntary, irregular tonic contractions of facial muscles supplied by the facial nerve (CN VII), most commonly affecting the orbicularis oculi. It typically begins in the 5th or 6th decade and is slightly more common in women. The spasms start in the orbicularis oculi and progressively spread to other facial muscles on the same side over months or years. Unlike focal dystonias, these contractions are synchronous in all affected muscles. Episodes last up to one minute, but the frequency and severity increase over time, significantly impacting quality of life. Triggers include stress and fatigue.
Causes include post Bell’s palsy sequelae, vascular compression (most common cause), brainstem pathologies like MS and brainstem tumors, idiopathic causes.
Hemifacial spasm treatment?
Treatment Approaches
1. Pharmacological Therapy:
• Anticonvulsants (e.g., benzodiazepines): Reduce the hyperexcitability threshold of nerve fibers, diminishing spasms.
2. Botulinum Toxin Injections (First-Line Therapy):
• Targets affected muscles to induce temporary paralysis, preventing excessive contraction.
• Provides effective symptom relief for 3-6 months, but requires repeat injections.
3. Microvascular Decompression (Definitive Treatment for Vascular Compression Cases):
• Surgical repositioning of the compressing artery/vein using Teflon padding to relieve pressure on CN VII.
• Invasive but provides long-term resolution.
What is the glossopharyngeal nerve?
The glossopharyngeal nerve (CN IX) is a mixed cranial nerve, carrying sensory, motor, and autonomic (parasympathetic) functions. It originates from the lateral medulla, just rostral to the vagus (CN X) and accessory (CN XI) nerves and exits the skull through the jugular foramen. At this point, it forms two ganglia: the superior ganglion and the inferior (petrous) glossopharyngeal ganglion. Due to its anatomical course, CN IX is closely related to the carotid artery and jugular vein, making vascular abnormalities possible causes of dysfunction.
- Motor Function (Yellow Fibers):
• Arises from the nucleus ambiguus and receives contralateral cortical input.
• Innervates the stylopharyngeus muscle, aiding in pharynx elevation and constriction (important for swallowing). - Sensory Function (Light Blue Fibers):
• Taste sensation from the posterior 1/3 of the tongue.
• General sensory information from the upper pharynx, tonsils, Eustachian tube, and tympanic membrane.
• Baroreceptor input from the carotid sinus and chemoreceptor input from the carotid body (conveyed to the nucleus solitarius for autonomic regulation). - Parasympathetic (Autonomic) Function (Red Fibers):
• Originates from the inferior salivary nucleus.
• Passes through both ganglia and synapses at the otic ganglion before innervating the parotid gland (stimulating salivation).
Clinical signs and symptoms include : dysphagia, unilateral reduced salivation, impaired gag reflex.
What is the vagus nerve?
The vagus nerve (CN X) is the largest visceral afferent nerve and a major parasympathetic nerve, playing a crucial role in autonomic regulation. It originates from the medulla oblongata, exits through the jugular foramen, and runs alongside CN IX (glossopharyngeal) and CN XI (accessory nerve). The vagus nerve innervates multiple structures, including the larynx, pharynx, heart, lungs, and digestive tract, making it essential for vocalization, swallowing, and autonomic functions.
Anatomy and Fiber Types. The vagus nerve has two main ganglia in its course:
• Jugular ganglion (sensory).
• Nodose ganglion (visceral sensory).
It branches into:
• Auricular branch (external ear).
• Meningeal branch (posterior fossa dura mater).
• Pharyngeal branch (soft palate and pharynx).
• Laryngeal branch (larynx).
Symptoms and signs of lesions include : vocalization impairment, dysphagia, weak cough, HR abnormalities and digestive issues.
Diseases include vasovagal attack, vagus nerve irritation.
What is the accessory nerve?
The accessory nerve (CN XI) is a motor nerve that innervates the sternocleidomastoid (SCM) and trapezius muscles, playing a crucial role in head rotation, shoulder elevation, and scapular movement.
Anatomy, the accessory nerve has two origins:
1. Cranial root (internal ramus):
• Arises from the caudal portion of the nucleus ambiguus.
• Joins the vagus nerve (CN X) to supply the larynx.
• This part is minor and often considered a branch of CN X.
2. Spinal root (external ramus):
• Major component of CN XI.
• Originates from the accessory nucleus in the upper cervical spinal cord (C1-C6).
• Ascends through the foramen magnum, exits via the jugular foramen, and innervates:
• Sternocleidomastoid: Rotates the head contralaterally.
• Trapezius: Elevates and stabilizes the scapula.
Associated to syringomelia, ALS, herpes zoster.
What is the hypoglossal nerve?
The hypoglossal nerve (CN XII) is a purely motor nerve responsible for the movement of the tongue. It controls intrinsic and extrinsic tongue muscles, ensuring proper articulation, swallowing, and food manipulation.
Muscles Innervated by CN XII
1. Styloglossus → Retracts and elevates the tongue (forms a trough for swallowing).
2. Hyoglossus → Depresses and retracts the tongue, making the dorsum more convex.
3. Genioglossus → Protrudes the tongue
Tongue Deviation:
• Unilateral CN XII lesion → Tongue deviates toward the affected side upon protrusion.
• Bilateral CN XII lesion → Severe speech and swallowing difficulties
What are bulbar and pseudo bulbar palsy?
Palsy is a condition caused by direct damage to the cranial nerve nuclei or the cranial nerves themselves, leading to lower motor neuron dysfunction. The most common causes include medullary lesions (tumors, infections, inflammation), Guillain-Barré Syndrome, neuromuscular junction disorders (such as myasthenia gravis), and primary muscle diseases. Clinically, it presents with nasal dysarthria, dysphagia with nasal regurgitation, tongue wasting with fasciculations, slow tongue movements, impaired swallowing, and absent palatal and pharyngeal reflexes.
In contrast, Pseudobulbar Palsy results from upper motor neuron (UMN) dysfunction, specifically from bilateral damage to corticobulbar tracts connecting the motor cortex to the cranial nerve nuclei. This condition often occurs due to bilateral strokes, neurodegenerative diseases, or brainstem demyelination. Symptoms include dysarthria with slow and limited tongue movements (but no early atrophy or fasciculations), exaggerated reflexes (such as hyperactive jaw jerk), frontal release signs, inappropriate spasmodic laughing or crying (emotional lability), and paraparesis.
What is CN III? Function? Lesions?
CN III, or the Oculomotor Nerve, is responsible for most eye movements, as well as pupil constriction and eyelid elevation. It is a mixed nerve, carrying motor and parasympathetic fibers.
Functions of the Oculomotor Nerve
1. Motor Function (Somatic Efferent)
Controls most of the extraocular muscles, which move the eyeball:
• Superior Rectus → Elevates the eye.
• Inferior Rectus → Depresses the eye.
• Medial Rectus → Adducts the eye (moves it inward).
• Inferior Oblique → Extorsion, elevation, and abduction of the eye.
• Levator Palpebrae Superioris → Elevates the upper eyelid.
- Parasympathetic Function (Visceral Efferent)
• Controls the pupil and lens accommodation via the Edinger-Westphal nucleus.
• Pupillary constriction: Activates the sphincter pupillae muscle (light reflex).
• Lens accommodation: Activates the ciliary muscle to focus on near objects.
A lesion affecting CN III can lead to:
1. “Down and Out” Eye Position → Due to unopposed action of lateral rectus (CN VI) and superior oblique (CN IV).
2. Ptosis (drooping eyelid) → Loss of levator palpebrae superioris function.
3. Mydriasis (pupil dilation) → Loss of parasympathetic innervation.
4. Loss of Accommodation → Difficulty in focusing on near objects.
Cranial nerve syndromes?
Cranial nerve syndromes are important for diagnosing conditions affecting the brainstem, skull base, or peripheral nervous system. They often present with specific patterns of cranial nerve involvement, which helps localize lesions. One important example is:
• Tolosa-Hunt Syndrome → Painful ophthalmoplegia caused by inflammation in the cavernous sinus or superior orbital fissure.
• Sphenoidal fissure syndrome —> opthalmoplegia caused by tumors or inflammation.
• Gardenigo syndrome —> otitis media + facial pain + diplopia caused by middle ear infections.
• Internal Acoustic Meatus syndrome —> facial weakness + hearing loss + vertigo due to vestibular schwannoma, meningioma or viral infections.
Brainstem syndromes?
Brainstem syndromes are critical in cerebrovascular diseases because they involve infarcts in the vertebrobasilar circulation, affecting multiple cranial nerves and long tracts. Here are key syndromes classified by brainstem region :
• Weber syndrome —> medial midbrain syndrome causing ipsilateral oculomotor palsy and contralateral hemiparesis due to paramedian branches of posterior cerebral artery occlusion.
• Benedikt syndrome —> ipsilateral oculomotor palsy, contralateral tremor and Parkinsonian like features due to paramedian PCA branches occlusion.
• Parinaud syndrome —> paralysis of vertical gaze and pupillary abnormalities due to pineal tumors, hydrocephalus or stroke affecting dorsal midbrain.
•
Pontine syndromes?
• Foville syndrome —> Ipsilateral horizontal gaze palsy and ipsilateral facial paralysis caused by occlusion of branches of basilar artery.
• Wallenberg syndrome —> contralateral deficits of spinothalamic pathway + Horner syndrome due to occlusion of vertebral artery.
• Dejerine syndrome —> presents as ipsilateral CN XII palsy with contralateral hemiplegia due to occlusion of vertebral artery.
What is anisocoria?
Anisocoria is defined as pupillary asymmetry, one pupil is more dilated/more constricted than the other.
Anisocoria in bright light : This is a parasympathetic deficit leading to a constriction deficit. Causes can be multiple and due to lesions in different locations:
- Sphincter pupillae damage.
- Pharmacologic dilation.
- Postganglionic lesion – ciliary nerves: Adie tonic pupil, tonically dilated pupil that reacts slowly to
light.
- Preganglionic lesion (III nerve palsy).
Anisocoria in dim light : This is a sympathetic deficit leading to a dilation deficit. Causes include:
- Physiological anisocoria.
- Mechanical anisocoria (e.g., trauma, surgical interventions).
- Hyperactivity of the sphincter pupillae.
- Horner’s syndrome: drooping of the eyelid (ptosis) + constriction of the pupil (miosis => failure of the dilator pupillae) + apparent enophtalmos.
What is papilloedema?
It is the most common cause of optic disc swelling without vision loss. It is caused by increased intracranial pressure as a result of:
• increase production of CSF (e.g., choroid plexus papilloma)
• blocks CSF flow in the ventricles or subarachnoid space (e.g., aqueduct stenosis)
• inhibited CSF drainage by arachnoid villi (e.g., blood or protein blockage due to infection, sarcoidosis, carcinomatous meningitis)
• intracranial mass (e.g., tumor, abscess, or hemorrhage)
• decreased flow of venous blood through the dural sinuses (e.g., venous sinus thrombosis)
• idiopathic intracranial hypertension.
Clinically it is characterized by transient binocular visual obscurations of the peripheral portion of our visual field. There also may be diplopia.
CN IV?
Trochlear nerve.
Anatomy—> It originates in the dorsal midbrain. The fascicle passes laterally to the aqueduct and exits the midbrain dorsally. The nerves cross before passing around the midbrain tectum to reach the free end of the tentorium and then pass forward into the wall of the cavernous sinus. The nerve enters to orbit through the superior orbital fissure and innervates the contralateral superior oblique muscle.
Clinical features —> Vertical diplopia with tilting of objects (torsional diplopia) which is worse on looking down and is caused by ipsilateral superior oblique weakness. Elevation of the affected eye (overaction of the inferior oblique) and head tilt away from the side of the lesion.
CNVΙ?
Anatomy —> It is located in the caudal paramedian pontine tegmentum beneath the floor of the IV ventricle. The fascicle has a long intrapontine course. It emerges from the brainstem ventrally and traverses the subarachnoid space in close relationship to the anterior inferior cerebellar artery. It runs within the cavernous sinus, before passing through the annular segment of the superior orbital fissure to innervate the lateral rectus muscle.
Clinical features —> horizontal diplopia due to ipsilateral rectus paresis with a primary position esotropia.
