Cranial Nerves Flashcards
(28 cards)
What are the 12 cranial nerves?
Olfactory, Optic, Oculomotor, Trochlear, Trigeminal, Abducens, Facial, Vestibulo-cochlear, Glossopharyngeal, Vagus, Accessory, Hypoglossal.
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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 (CN V) is the largest cranial nerve and has both sensory and motor components. It originates from the pons with a large sensory root and a smaller motor root. The trigeminal (Gasserian) ganglion, located in Meckel’s cave, contains the sensory neuron cell bodies. CN V divides into three branches: ophthalmic (V1), maxillary (V2), and mandibular (V3).
Sensory components: The sensory root carries information from the face, scalp, cornea, nasal and oral cavities, meninges, and teeth. Sensory fibers project to three trigeminal nuclei: (1) Principal sensory nucleus (pons) – fine touch and proprioception. (2) Spinal nucleus (extends to C3) – pain and temperature. (3) Mesencephalic nucleus (midbrain) – jaw proprioception (e.g., jaw jerk reflex).
Motor components: The motor nucleus of CN V is in the pons and receives bilateral corticobulbar input. Motor fibers bypass the ganglion and travel in V3 to innervate the muscles of mastication (masseter, temporalis, pterygoids), mylohyoid, anterior digastric, tensor tympani, and tensor veli palatini.
Branches of CN V:
V1 (ophthalmic) – sensory; exits via the superior orbital fissure; innervates the forehead, scalp, upper eyelid, cornea, nasal bridge, and meninges.
V2 (maxillary) – sensory; exits via the foramen rotundum; innervates the lower eyelid, cheek, upper lip, upper teeth, nasal cavity, maxillary sinus, and meninges.
V3 (mandibular) – both sensory and motor; exits via the foramen ovale; sensory to lower lip, chin, jaw, lower teeth, and anterior two-thirds of the tongue (somatic sensation only); motor to the muscles listed above.
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 with motor, sensory, and parasympathetic functions. It arises from the pons and loops around the abducens nucleus before exiting at the cerebellopontine angle. It travels with CN VIII through the internal acoustic meatus, then enters the facial canal. There, it gives off:
• Greater petrosal nerve → lacrimal gland (parasympathetic)
• Chorda tympani → taste (anterior 2/3 tongue) + salivation (submandibular/sublingual glands)
• Stapedial nerve → stapedius muscle (reduces sound sensitivity)
It exits the skull via the stylomastoid foramen, then gives motor branches to muscles of facial expression:
• Temporal, zygomatic, buccal, marginal mandibular, cervical
Also gives the posterior auricular nerve (scalp + 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). The nerve fibers regrow to the wrong targets
• 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 nerve with motor, sensory, and parasympathetic functions. It arises from the lateral medulla, exits the skull via the jugular foramen, and forms two ganglia (superior and inferior). It travels near the carotid artery and jugular vein.
Motor: Innervates stylopharyngeus, which elevates the pharynx during swallowing.
Sensory: Carries:
• Taste from the posterior 1/3 of the tongue
• General sensation from the pharynx, tonsils, tympanic membrane, Eustachian tube
• Baro/chemoreceptor input from carotid sinus/body → nucleus solitarius
Parasympathetic: From inferior salivatory nucleus → via otic ganglion → parotid gland (salivation)
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?
Bulbar palsy refers to lower motor neuron (LMN) dysfunction affecting cranial nerves that arise from the medulla oblongata — specifically CN IX, X, XI, and XII. These nerves control swallowing, speech, palatal movement, and tongue function. Causes include medullary lesions (tumors, inflammation, infections), Guillain-Barré syndrome, neuromuscular junction disorders (e.g., myasthenia gravis), and primary muscle diseases. Clinical features include nasal dysarthria, dysphagia with nasal regurgitation, tongue wasting and fasciculations, weak or absent palatal and pharyngeal reflexes, and slow, weak tongue movement.
Pseudobulbar palsy, in contrast, is due to upper motor neuron (UMN) lesions of the corticobulbar tracts — which connect the cerebral cortex to the cranial nerve nuclei bilaterally. It typically results from bilateral strokes, neurodegenerative disease, or brainstem demyelination. Symptoms include spastic dysarthria, slow tongue movement without atrophy, hyperactive jaw jerk reflex, emotional lability (involuntary laughing or crying), and often frontal release signs. Gag reflex may be brisk rather than absent.
