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Neurology Chapter 1 General Introduction to Neurology 002
Neurology Chapter 1: Neurology General Thought Map, including the basic structure of the nervous system, Basic characteristics of nervous system damage, localization and diagnosis of nervous system damage, etc.
Edited at 2024-03-25 23:41:44
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Neurology Chapter 1 General Introduction to Neurology 002
- Valentine's Day marketing campaign
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- Milano Cortina 2026 Ice Hockey Schedule
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Neurology Chapter 1 General Introduction to Neurology 002
Section 1 Overview
basic structure of nervous system
nerve cells
Neuron: cell body, dendrites, axon (cord)
Glial cells
Macroglia: oligodendrocytes (form myelin sheath), astrocytes, ependymal cells
Microglia
nerve fibers
Myelinated fibers: oligodendrocytes (central nervous system), Schwann cells (peripheral nerves)
unmyelinated fibers
Basic characteristics of nervous system damage
Description by symptoms and signs
Irritation symptoms: refer to over-excitability caused by irritation of nerve structures (such as epilepsy, sciatica)
Deletion symptoms: refers to the weakening/disappearance of the normal function of the corresponding control area when the neural structure is damaged.
Release symptoms: after the high-level center is damaged, the low-level center originally inhibited by it becomes hyperfunctional due to the release of inhibition.
∎ Loss of communication symptoms/disconnection shock symptoms: refers to the acute and severe local damage to the central nervous system, which causes the temporary loss of neurological function in remote parts that are closely related to the damaged part; such as brain shock and spinal cord shock; when shock After the period, functional deficit symptoms/release symptoms of damaged structures often appear gradually.
According to the scope of the disease
Focal disease: but can appear multifocal (same lesion in multiple locations)
diffuse disease
Systemic disease: mainly limited to a certain neuroanatomical system
Section 2: Localization and Diagnosis of Nervous System Damage
1. Cranial nerves
(1) Olfactory nerve (Ⅰ)
Anatomy and Physiology
Special visceral sensory nerves: olfactory cells → olfactory filaments/olfactory nerves → ethmoid foramen → telencephalic olfactory bulbs → olfactory tracts → lateral olfactory striae → olfactory center (some also pass through the medial olfactory striae/middle olfactory striae → inferior corpus callosum gyrus/anterior perforated substance)
Function: conduct smell
Features: The only sensory pathway that directly transmits nerve impulses to the cortex without exchanging neurons in the thalamus
Lesion location
Olfactory center lesions: Unilateral lesions generally do not cause loss of smell (∵ bilateral communication); irritating lesions of the olfactory center can cause olfactory hallucination attacks
Olfactory nerve, olfactory bulb, and olfactory tract lesions: olfactory disorder
Local lesions in the nasal cavity: bilateral hyposmia/absence
(2) Optic nerve (Ⅱ)
Anatomy and Physiology
Special somatosensory nerves: bipolar cells (level 1 neurons) → retinal ganglion cells → optic nerve → optic foramen → optic chiasm (only the nasal side fibers cross, not the temporal side) → optic tract → ① lateral geniculate body → optic Radiation → striatal area;
② Superior colliculus arm → superior midbrain/pretectal area → E-W nuclei on both sides → oculomotor nerve → ciliary ganglion → postganglionic fibers → pupillary sphincter (pupillary light reflex)
Function: conduct vision
Lesion location
Visual impairment and visual field defects
Retinal damage: central blind spot
Optic nerve damage: ipsilateral vision loss/total blindness (sudden blindness → arterial occlusion; central visual field defect → papillitis, retrobulbar optic neuritis; peripheral visual field defect, physiological blind spot expansion → intracranial hypertension; irregular visual field defect → optic nerve compression Sexual lesions; tubular visual field → hysteria, visual fatigue)
Chiasmatic damage: lateral damage (such as severe sclerosis of the internal carotid artery) → visual field defect on the nasal side of the ipsilateral eye; damage to the middle part (such as intrasellar tumor) → temporal hemianopia of both eyes; overall damage (such as pituitary tumor stroke) → totally blind
(One side) Optic tract damage: homonymous hemianopia in the contralateral visual field of both eyes, loss of direct light reflex in the pupil on the hemianopic side
Visual radiation damage: total damage (lesion involving the posterior limb of the internal capsule) → homonymous hemianopia in the contralateral visual fields of both eyes (but normal light reflex); damage to the lower part (lesions in the posterior temporal lobe) → homonymous hemianopia in the contralateral visual fields of both eyes Upper quadrantopia; upper damage (parietal lobe lesions) → isotropic lower quadrantopia in the contralateral visual field of both eyes
Visual center damage: localized damage on one side → homonymous quadrantopia on the contralateral side of both eyes; complete damage on one side → homonymous hemianopia on the contralateral visual field of both eyes (but normal light reflex and macular avoidance); irritant damage → Flashing visual hallucinations in the contralateral visual field of both eyes
Optic papilla abnormalities
Papiledema: seen in various diseases that cause increased intracranial pressure
Optic atrophy: vision loss/disappearance, pupil dilation, light reflex weakening/disappearance
(3) Oculomotor nerve (III), trochlear nerve (IV), abducens nerve (VI)
Anatomy and Physiology
Oculomotor nerve: arises from the oculomotor nucleus of the superior colliculus of the midbrain; includes motor fibers and parasympathetic components
Lateral nucleus → motor fibers → interpeduncular fossa → between the posterior cerebral artery and the superior cerebellar artery → lateral wall of the cavernous sinus → superior orbital fissure → the upper branch innervates the levator palpebrae superioris and superior rectus muscles, and the lower branch innervates the medial rectus and inferior rectus muscles. Oblique muscle, inferior rectus muscle
Median nucleus/Perlia nucleus→parasympathetic component→medial rectus muscle (vergence movement)
∎Accessory nucleus/Eye-Wei (E-W) nucleus→parasympathetic component preganglionic fibers→ciliary ganglion→postganglionic fibers→pupillary sphincter, ciliary muscle (miosis and accommodation reflex)
Trochlear nerve: motor fibers; trochlear nerve nucleus of the inferior midbrain colliculus → crosses in the medullary velum and exits the brain → lateral wall of the cavernous sinus → superior orbital fissure → superior oblique muscle
Abducens nerve: motor fibers; abducens pontine nucleus → medial part of the pontomal sulcus → lateral wall of the cavernous sinus → superior orbital fissure → lateral rectus muscle
Eye movement: lateral rectus → lateral; medial rectus → medial; superior oblique → lateral and inferior; inferior oblique → lateral and superior; superior rectus → medial and superior; inferior rectus → medial and inferior; the coordination of eye movements is through Medial longitudinal fasciculus
Lesion location
Eye muscle damage in different parts
Peripheral ophthalmoplegia: combined paralysis of the three major nerves is common, especially cavernous sinus thrombosis and superior orbital fissure syndrome
Oculomotor nerve palsy: Complete damage manifests as ptosis, outward and downward strabismus (limited upward, inward, and downward movement), diplopia, mydriasis, and loss of light reflex/accommodative reflex.
Trochlear nerve palsy: often combined with oculomotor nerve palsy; simple damage is manifested by the upward position of the eyeball (limited outward and downward movement), diplopia when looking outward and downward, and the head is often tilted to the opposite shoulder
Abducens nerve palsy: esotropia (limited outward movement), diplopia when both eyes look toward the affected side
Nuclear ophthalmoplegia: similar to peripheral ophthalmoplegia; but has the following characteristics
Bilateral eye movement disorders: especially the oculomotor nucleus
Damage to adjacent brainstem structures: For example, damage to the abducens nucleus may involve facial nerve fibers, trigeminal nerve, and pyramidal tract.
Dissociated ophthalmoplegia: manifests as selective damage to individual nerve nuclei, which can only involve some of the nuclei and cause involvement of certain eye muscles, leaving other eye muscles unaffected; seen in oculomotor nuclear palsy
Internuclear ophthalmoplegia: the lesion damages the medial longitudinal fasciculus of the brainstem (medial longitudinal fasciculus syndrome): more common in brainstem lacunar infarction and multiple sclerosis
Anterior internuclear ophthalmoplegia: The lesion is located in the ascending fibers of the medial longitudinal fasciculus between the lateral visual center of the pons and the oculomotor nucleus; manifested by the inability of the eyeball on the affected side to adduct when looking toward the contralateral side of the lesion. The lateral eyeball can abduct but is accompanied by monocular tremor, and the convergence reflex is normal.
Posterior internuclear ophthalmoplegia: The lesion is located in the descending fibers of the medial longitudinal fasciculus between the lateral visual center of the pons and the abducens nerve nucleus; manifested by the inability of the eyeball on the affected side to abduct when looking toward the same side as the lesion, while the eyeball on the contralateral side can move inward. When the vestibule is stimulated, the affected side may abduct normally and the convergence reflex is normal.
One and a half syndrome: Lesion of the pontine tegmentum on one side causes simultaneous involvement of the lateral visual center of the pons and the medial longitudinal fasciculus of the contralateral side that has crossed over and communicates with the medial rectus nucleus of the oculomotor nerve on the same side; manifested as when the eyeball of the affected side is gazed horizontally Can neither adduct nor abduct. The contralateral eye cannot adduct when looking horizontally and has horizontal tremor when abducting.
Supranuclear ophthalmoplegia/central ophthalmoplegia: Same-direction gaze movement/joint movement (gaze) disorder in both eyes; Characteristics: ① Both eyes are affected at the same time; ② No diplopia; ③ Reflexive movements are still preserved
It means that the patient's eyes cannot move to one side at will, but when a sound suddenly occurs on that side, the eyes can reflexively turn to that side; this is because the temporal lobe has fibers that are connected to the III, IV, and VI cranial nerves.
Anatomical basis: The lateral vision center (gaze center) of the cerebral cortex is located in the posterior part of the middle frontal gyrus, the vertical movement center of the two eyes is located in the midbrain, and the horizontal gaze center is located in the pons (cross control)
Horizontal gaze paralysis
Damage to the lateral gaze center of the cerebral cortex - lateral gaze paralysis of both eyes: Destructive lesions may cause paralysis of the contralateral gaze of both eyes and hemitropia on the affected side; irritating lesions may cause contralateral hemitropia of both eyes.
Damage to the lateral visual center of the pons: Damage to the connection fibers with the middle frontal gyrus → Gaze on the affected side of both eyes; Damage to the lateral visual center of one side of the pons → Paralysis of gaze on the affected side of both eyes and contralateral hemitropia
Vertical Gaze Paralysis
Upper half of the superior colliculus: Destructive lesions may cause inability to gaze upward in the same direction (Parinaud syndrome); irritating lesions (such as post-encephalitis parkinsonism, use of metoclopramide/phenothiazines) may cause paroxysmal binocular vision Turning upward (ocular crisis)
Lower half of the superior colliculus: Destructive lesions appear and the eyes cannot gaze downward in the same direction.
Diplopia caused by different ophthalmoplegias
Double vision: refers to when a certain extraocular muscle is paralyzed, the movement of the eyeball in the direction of contraction of the paralyzed muscle is unable/restricted, resulting in double vision (the healthy eye can project the image of external objects to the macular area as a real image/real image, The affected eye can project the image of external objects onto the retina outside the macular area as a virtual image/false image)
Imaging rules: ① When one side of the lateral rectus muscle is paralyzed, the eyeball moves inward, and the virtual image is located outside the real image; ② When one side of the medial rectus muscle is paralyzed, the eyeball moves outward, and the virtual image is located inside the real image; ③ Paralysis of the extraocular muscles that control the upward movement of the eyeball When the eyeball moves downward, the virtual image is located above the real image; ④ When the extraocular muscles that control the downward movement of the eyeball are paralyzed, the eyeball moves upward, and the virtual image is located below the real image; ⑤ Summary: The most obvious direction of diplopia occurs when the paralyzed muscles act in the direction of force
Pupil changes caused by damage to different parts
∎Pupillary size: "Jiao Da and Xiao"; the normal diameter is 2.5~3.5mm
Micromiosis (diameter <2.5mm): seen in upper cervical sympathetic nerve damage (one side is seen in Horner syndrome, and bilateral is seen as pinpoint pupils)
Manifested by narrowing of the eye fissure, miosis of the pupil, enophthalmos, and reduction/disappearance of facial sweating on the affected side; seen in C8~T1 segment injuries
Mydriasis (diameter >5mm): seen in oculomotor nerve palsy
Abnormal pupillary light reflex: Pay attention to the absence of pupil dilation and loss of light reflex when the lateral geniculate body and its pathways are affected
Abnormal collective reflex
Vergence reflex: retina → optic nerve → chiasm → optic tract → lateral geniculate body → striatal area → pretectal area → median nucleus of the oculomotor nerve → medial rectus muscles of both eyes → binocular convergence; loss is more common in Parkinson's disease , midbrain lesions
Accommodative reflex: retina → optic nerve → chiasm → optic tract → lateral geniculate body → striatal area → pretectal area → oculomotor nerve E-W nucleus → pupillary sphincter and ciliary muscle of both eyes → miosis; loss is more common in diphtheria ,encephalitis
Argyll-Robertson pupil: The pupils on both sides are small, unequal in size, and have irregular edges. The light reflex disappears but the accommodative reflex exists. It is caused by damage to the light reflex pathway in the anterior area of the midbrain. Caused, common in neurosyphilis
Adie’s pupil/tonic pupil: more common in middle-aged women; characterized by dilated pupil on one side, loss of light reflex when examined under ordinary light, but the pupil may appear slow when exposed to strong light continuously in the dark Contraction, then slowly dilates after the light stops; the pupil also shows slow contraction when adjusting the reflex; accompanied by weakening/absence of systemic tendon reflexes; when accompanied by segmental anhidrosis and orthostatic hypotension, it is called Eddie's syndrome
(4) Trigeminal nerve (V)
Anatomy and Physiology
Sensory nerve fibers/general somatic sensation: trigeminal nerve semilunar (pseudo-unipolar neurons); one end continues through the superior orbital fissure, round foramen, and foramen ovale to become the ophthalmic nerve, maxillary nerve, and mandibular nerve; one end is connected to the trigeminal nerve Brain nucleus (deep sensation), spinal trigeminal tract nucleus (pain and temperature sensation; upper part is perioral, lower part is periauricular), trigeminal sensory main nucleus (tactile), composed of 2nd-level neurons of the main sensory nucleus and spinal tract nucleus The fibers that originate cross to the opposite side to form the trigeminal lemniscus → ventromedial ventral nucleus of the thalamus → posterior limb of the internal capsule → lower 1/3 of the postcentral gyrus
Motor nerve fibers/special visceral movements: pontine trigeminal motor nucleus → runs in the mandibular nerve → innervates the masticatory muscles and tensor tympani muscle
Corneal reflex: cornea → trigeminal ophthalmic nerve → trigeminal semilunar ganglion → trigeminal nerve main sensory nucleus → bilateral facial nerve nuclei → facial nerve → orbicularis oculi muscle contraction (eye closing reaction)
Lesion location
Peripheral damage to the trigeminal nerve
Irritant lesions: trigeminal neuralgia
Destructive lesions: weakened/disappeared sensation in the distribution area of the trigeminal nerve, paralysis of masticatory muscles, deviation of the mandible to the affected side when opening the mouth
Trigeminal nucleus damage
① Sensory nucleus (trigeminal spinal tract nucleus): ① dissociative sensory disorder: pain and temperature sensation disappears but touch/deep sensation exists; ② onion skin-like distribution: perioral sensory disturbance occurs in upper damage, and periauricular/perifacial sensation occurs in lower damage sensory impairment
Motor nucleus: Weakness/paralysis of the masticatory muscles on the same side, and the mandible is deflected to the affected side when opening the mouth
(5) Facial nerve (VII)
Anatomy and Physiology
Motor fibers: Facial nerve nucleus in the lower part of the pons → Bypass the abducens nerve nucleus → Lateral part of the pontine sulcus → Inner ear foramen → Facial nerve canal → Cross the geniculate ganglion → Send out the stapedius nerve and chorda tympani nerve along the way → Stylomastoid foramen → Pass through Parotid gland → innervates facial muscles except masticatory muscles and levator palpebrae superioris muscle (bilateral innervation of upper facial muscles, contralateral innervation of lower facial muscles), ear muscles, occipital muscles, platysma muscles, and stapedius muscles
sensory fibers
∎ Taste fibers: special visceral sensation; geniculate ganglion, peripheral processes form the chorda tympani nerve, join the lingual nerve, and provide taste in the anterior 2/3 of the tongue; the central process forms the intervening nerve of the facial nerve, and terminates in the solitary tract with the glossopharyngeal nerve taste fibers The tract nucleus → crosses to the opposite side → ascends medially to the medial lemniscus and terminates in the lateral thalamic nucleus → the lower part of the postcentral gyrus
General somatosensory: geniculate ganglion; receives sensation from the tympanic membrane, inner ear, external ear, and skin of the external auditory canal
Parasympathetic nerve fibers: general visceral movement; superior salivary nucleus → intermediary nerve → ① chorda tympani nerve → lingual nerve → submandibular ganglion → postganglionic fibers innervate sublingual gland and submandibular gland; ② greater petrosal nerve → pterygopalatine ganglion → ganglion Posterior fibers innervate lacrimal gland
Lesion location
Central facial paralysis VS peripheral facial paralysis
Further localization and diagnosis of peripheral facial paralysis
Anterior facial nerve canal damage
Facial nerve nucleus damage: peripheral facial nerve palsy; often accompanied by abducens nerve palsy and contralateral pyramidal tract sign
Damage to the geniculate ganglion: peripheral facial paralysis, anterior 2/3 of the tongue, dysgeusia, lacrimal gland/salivary gland secretion disorder; Hunt syndrome may be present
Intrafacial nerve canal damage: peripheral facial paralysis, anterior 2/3 of the tongue, dysgeusia, salivary gland secretion disorder; may be accompanied by hyperacusis (suggesting that the lesion is above the stapedius muscle nerve)
Damage outside the stylomastoid foramen: only peripheral facial paralysis occurs
(6) Vestibulocochlear nerve (VIII)
Anatomy and Physiology
Cochlear nerve: special somatosensory; organ of Corti→internal cochlear ganglion (level 1 neuron)→cochlear nerve→inner ear foramen→lateral part of the pontine sulcus→anterior and posterior nuclei of the pontine cochlear nerve→part of it crosses to the opposite side via the trapezoid, and the other Part of the ipsilateral ascending → lateral lemniscus → inferior colliculus (auditory reflex), medial geniculate body → auditory radiation → cortical auditory center
Vestibular nerve: special somatosensory; utricle/sacculus/ampullary → vestibular ganglion of inner ear → vestibular nerve → foramen of inner ear
→Lateral part of the pontomonal sulcus→Pontine/medulla oblongata vestibular nuclei group→①Inferior cerebellar peduncle→Flomer bulb; ②Vestibulospinal tract→ipsilateral anterior horn cells; ③Medial longitudinal fasciculus
Lesion location
cochlear nerve
Deafness
Tinnitus
Definition: hearing a ringing sensation without any external sound source stimulation
Classification: Subjective tinnitus (no objective findings), objective tinnitus
Characteristics: Tinnitus caused by neurological diseases is mostly high-pitched, while lesions of the outer ear/middle ear are mostly low-pitched.
Hyperacusis
Definition: The patient perceives normal sounds as being stronger than the actual sound source.
Seen in: early stage of otitis media, stapedius muscle paralysis caused by facial nerve paralysis
vestibular nerve
Vertigo
Definition: It is a motion/positional illusion, which causes the spatial relationship between people and the surrounding environment to be distorted in the cerebral cortex, resulting in feelings of rotation, tilting, and ups and downs; there is only a general sense of motion sickness but no awareness of the spatial position of oneself/the external environment. pseudovertigo
Classification
Systematic
Non-systemic: characterized by dizziness, unsteady standing, usually no sense of external environment/self rotation, or swaying, rarely accompanied by nausea and vomiting (pseudovertigo); common in eye diseases, cardiovascular system diseases, endocrine and metabolic diseases, Poisoning, infection, anemia
Nystagmus
balance disorder
(7) Glossopharyngeal nerve (IX), vagus nerve (X)
Anatomy and Physiology
Glossopharyngeal nerve
Special visceral sensation: taste buds in the back 1/3 of the tongue → inferior ganglion → nucleus of the solitary tract
General visceral sensation: pharynx, tonsils, posterior 1/3 of tongue, Eustachian tube, tympanic mucosa → inferior ganglion → nucleus of solitary tract
General somatosensory: skin behind the ear → superior ganglion → spinal trigeminal tract nucleus
Special visceral movement: nucleus ambiguus → jugular foramen → innervates stylopharyngeal muscle (completes swallowing together with vagus nerve)
Parasympathetic fibers/general visceral movement: inferior salivary nucleus → tympanic nerve, lesser petrosal nerve → auricular ganglion → parotid gland
Vagus nerve
General visceral sensation: throat, esophagus, trachea, thoracic and abdominal organs → inferior ganglion → nucleus of the solitary tract
General somatosensory: external auditory canal, concave skin of auricle, dura mater → superior ganglion → spinal trigeminal tract nucleus
Special visceral movements: nucleus ambiguus → jugular foramen → innervates the soft palate and striated muscles of the throat
Parasympathetic fibers/general visceral movement: dorsal nucleus of the vagus nerve → parasympathetic ganglion of the vagus plexus → postganglionic fibers control the activities of smooth muscles, myocardium, and glands in the thoracoabdominal cavity
Lesion location
Glossopharyngeal and vagus nerve joint damage
True bulbar palsy/bulbar palsy: When the glossopharynx and vagus nerve are damaged at the same time (lower motor neuron paralysis), hoarseness, difficulty swallowing, choking on drinking water, and loss of gag reflex will occur; when one side is injured, the symptoms are mild, and paralysis can be seen when opening the mouth. The lateral soft palate arch is lower, the palatal velum is biased to the opposite side, the soft palate lift is limited, the pharyngeal sensation is lost, and the gag reflex disappears
Pseudobulbar palsy/pseudobulbar palsy: caused by upper motor neuron paralysis; dysarthria and dysphagia occur only when bilateral corticobulbar tracts are damaged, but the gag reflex is present; common in vascular lesions of both cerebral hemispheres
Mandibular reflex: Instruct the patient to open his mouth slightly, and the examiner places his thumb in the center of the patient's mandible, and then taps his thumb lightly, causing the patient's mandible to lift rapidly; it is not easy for normal people to elicit
Separate damage to glossopharynx and vagus nerve
Glossopharyngeal nerve palsy: hypoesthesia in the pharynx, loss of gag reflex, loss of taste in the back 1/3 of the tongue, mild paralysis of the pharyngeal muscles
Vagal palsy: hoarseness, dysarthria, inability to lift the soft palate, difficulty swallowing, weak cough, tachycardia
(8) Accessory nerve (XI)
Anatomy and Physiology
Medulla branch: nucleus ambiguus → joins the vagus nerve → recurrent laryngeal nerve → controls vocal cord movement
Spinal branch: Ventrolateral cell column of the anterior horn of cervical spinal cord segments 1 to 6 → Foramen Magnum → Confluent with medullary branch → Jugular foramen → Innervates sternocleidomastoid and trapezius muscles
Lesion location
Accessory nerve nucleus/accessory nerve damage on one side: paralysis of the innervating muscles on the ipsilateral side → inability to turn the head to the opposite side, shoulder droop/shrug weakness on the affected side; posterior cranial fossa lesions are often damaged together with the vagus nerve and glossopharyngeal nerve (jugular foramen syndrome) )
Bilateral accessory nerve nucleus/accessory nerve damage: weakness in forward flexion of the head, difficulty in standing upright, backward position, and inability to raise the head when lying supine
(9) Hypoglossal nerve (XII)
Anatomy and Physiology
Medulla oblongata hypoglossal nucleus → hypoglossal canal → innervates tongue muscles
Note: only innervated by the contralateral corticobulbar tract
Lesion location
Supranuclear lesions of the hypoglossal nerve (central hypoglossal nerve palsy): When one side is damaged, the tongue is extended to the opposite side without tongue muscle atrophy or fasciculations.
Hypoglossal nerve and nuclear lesions: When one side is affected, the tongue muscle on the affected side is paralyzed, and the tongue is extended toward the affected side; when both sides are affected,
Limited tongue extension accompanied by tongue muscle atrophy and fasciculations