Тройничный нерв методы исследования, симптомы поражения

Main ideas and lessons

• The lecture explains how to objectively examine the trigeminal nerve and how to interpret symptoms when it is damaged, including both sensory and motor dysfunction.
• It then transitions to trigeminal neuralgia, a pain syndrome that can occur due to damage or compression of the trigeminal nerve (often without primary sensory loss).
• Finally, it covers motor-part lesions of the trigeminal nerve, which mainly affect the masticatory muscles and related reflexes.

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Methodology: step-by-step examination (trigeminal nerve)

1) Objective examination: palpation of branch exit points (face)

• Palpate the exit points of trigeminal nerve branches on the facial skin to identify tenderness (possible soreness).
• Key points:
  • Supraorbital notch → supraorbital nerve (described as nervus amicus)
  • Infraorbital canal → infraorbital nerve (described as nervus maxis)
  • Mandibular foramen → mandibular nerve

2) Sensitivity testing in trigeminal innervation zones

• Test sensation in the right and left innervation areas and compare them.

Pain sensitivity

• Use a blunt needle or a toothpick.

Temperature sensitivity

• Use test tubes with hot/cold water or a thermal tip/device.

Tactile (touch) sensitivity

• Use a brush.

Direction/coverage of sensory testing

• Test superficial sensitivity:
  • not only bottom-to-top (along the branch innervation zones),
  • but also across dermatomal “segmental” territories.

3) Segmental (dermatomal) testing

• Perform injections to map sensory involvement:
  • from the ear to the lips or to the tip of the nose, on each side.
• Purpose:
  • evaluate segmental distribution and help identify associated muscle issues.

4) Masticatory function and motor assessment

Chewing ability and muscle wasting

Assess:

• whether the patient has difficulty chewing
• atrophy of the temporal and masticatory (masseter) muscles
• deviation of the lower jaw when opening the mouth

Manual comparison of muscle tension

• Examiner places fingers on the temporal and masticatory muscles.
• Ask the patient to perform the relevant movements.
• Compare the degree of tension: right vs left

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Symptom patterns: sensory vs motor trigeminal lesions

A) Sensory pathway lesions (loss of sensation patterns)

Cortical end involvement

• Damage to the lower third of the postcentral gyrus (cortical sensory pathway end)
• → loss of sensitivity on the opposite half of the face
• Reason: sensory fibers cross in the brainstem.

Thalamic lesion

• If the thalamus is damaged (sensory relay area)
• → contralateral trigeminal sensory deficit
• Described as “counter-theraphy hemianesthesia” (wording is unclear/garbled in the text; meaning indicates contralateral hemi-anesthesia).

Brainstem spinal trigeminal nucleus (dissociation)

• Upper parts of the spinal tract nucleus:
  • supply internal facial skin regions (“Solder dermatomes” — term appears garbled)
• Lower parts of the nucleus:
  • supply external facial dermatomes
• If this nucleus is damaged:
  • facial anesthesia shows dissociation
  • affects only superficial sensitivity
  • follows a segmental dermatomal distribution, not trigeminal branch projection

Bulbous (“onion-ring”) pattern

• Upper/central involvement may cause sensory disorder resembling:
  • concentric circles (“onion rings”)
• Sometimes called the bulbar type (“bulbous type” in the text).

Alternating hemianesthesia

• If trigeminal sensory nuclear areas are damaged together with spinal tract involvement in the brainstem:
  • face superficial sensitivity disturbance occurs on the side of the lesion
  • trunk and limbs anesthesia occurs on the opposite side
• Reason stated: crossing of the spinothalamic tract in the spinal cord.
• Named syndrome:
  • Wallenberg–Zakharchenko syndrome
• Cause given:
  • ischemic lesion from disturbed blood flow in the vertebral artery / inferior posterior cerebellar artery (as described), affecting the dorsolateral area

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B) Lesions at different trigeminal levels (peripheral vs ganglion/root)

Trigeminal ganglion or trigeminal root lesion

• Anesthesia affects the entire same-named half of the face
• Scalp sensitivity can be involved
• Corneal/superciliary/mandibular reflexes may be impaired (especially corneal and other reflexes)

Isolated peripheral branch lesion (maxillary/ophthalmic/mandibular nerves)

• Sensory loss limited strictly to the innervation zone of that branch
• Described as peripheral-type facial disorder
• Corresponding reflexes may fade/suppress:
  • corneal reflex with ophthalmic branch involvement
  • mandibular reflex with mandibular involvement (as reflected in the text)

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Trigeminal neuralgia (pain syndrome despite trigeminal involvement)

• Triggered by trigeminal nerve damage or dysfunction; classic example is trigeminal neuralgia.
• Characteristics:
  • short attacks of severe shooting/piercing/cutting pain
  • usually affects one trigeminal branch, most often:
    • the second or third branch (maxillary/mandibular), sometimes multiple branches
  • trigger zones: pain provoked by touching sensitive facial areas
  • common provoking stimuli (examples given):
    • washing
    • shaving
    • brushing teeth
  • light interval between attacks (pain-free periods)
  • duration of one attack:
    • not more than ~2 minutes
  • often associated with muscle spasm on the affected side

Causes described (with mechanism)

• Most often: neurovascular conflict
  • vessels compress the trigeminal root, usually described as:
    • superior cerebellar artery
  • compression occurs at a vulnerable unmyelinated segment near the root after exiting the brainstem/pons
• MRI example etiologies mentioned:
  • Multiple sclerosis (plaques/foci in trigeminal root/spinal trigeminal nucleus region; contrast enhancement)
  • Cavernous malformation (compressing the right pons area, affecting root)
  • Primary CNS lymphoma
  • Inflammatory disease / herpes zoster
    • left-sided facial pain syndrome resembling trigeminal neuralgia

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Motor-part trigeminal lesions (masticatory muscle dysfunction)

What happens when motor fibers/nucleus are damaged

Lesion locations mentioned:

• motor nucleus in the pons
• peripheral motor fibers
• root of trigeminal nerve or mandibular nerve

Expected clinical result:

• flaccid paralysis/weakness of masticatory muscles on the same side (ipsilateral)

How it is examined

• Detect unilateral weakness by:
  • palpating temporal and masseter muscles
  • asking the patient to perform chewing movements
  • noting:
    • reduced/absent muscle contractions
    • atrophy of masticatory muscles
• Jaw deviation test:
  • when opening the mouth and trying to push the lower jaw forward:
    • jaw deviates toward the side of the lesion
  • reason: pull by the opposite pterygoid muscle

Bilateral damage

• Lower jaw “hangs down”
• Chewing and function become difficult (severe impairment implied)

Reflex changes

• Motor fiber damage:
  • accompanied by inhibition of the mandibular reflex

Main causes (as stated)

• Injuries or tumors affecting:
  • the motor nucleus or peripheral motor fibers

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Speakers / sources featured

• Speaker/lecturer: Not explicitly named (referred to indirectly via the lecture script).
• Clinical syndromes/conditions mentioned:
  • Wallenberg–Zakharchenko syndrome
  • Trigeminal neuralgia
• Neuroanatomical structures named:
  • Trigeminal nerve branches (supraorbital, infraorbital, mandibular)
  • Spinal tract nucleus of the trigeminal nerve
  • Thalamus and described sensory pathways
  • Spinothalamic tract
• Arterial structures mentioned:
  • Vertebral artery
  • Inferior posterior cerebellar artery (as described)
  • Superior cerebellar artery (neurovascular conflict)