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Neurology Chapter 1 General Introduction to Neurology 003
Neurology Chapter 1: Neurology General Thought Map, which introduces the localization and diagnosis of nervous system damage, sensory system, motor system, etc.
Edited at 2024-03-25 23:41:15
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Neurology Chapter 1 General Introduction to Neurology 003
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Neurology Chapter 1 General Introduction to Neurology 003
Section 2: Localization and Diagnosis of Nervous System Damage
2. Sensory system
Anatomy and Physiology
Classification of general feelings
Shallow sensation: pain, temperature, touch
Deep sense: movement sense, position sense, vibration sense
Composite sensation/cortical sensation: refers to the entity sense, graphic sense, two-point discrimination sense, positioning sense, and weight sense formed by analyzing, comparing, and integrating deep and shallow senses in the parietal cortex of the brain.
conduction pathway
Pain and temperature sensation: spinal nerve sensory fibers → spinal ganglion → lateral part of the posterior root → dorsal horn of the spinal cord → cross to the contralateral lateral funiculus via the anterior commissure of the white matter → lateral spinothalamic tract → ventroposterolateral nucleus of the thalamus → thalamocortical tract → postcentral The upper part of the gyrus and the posterior part of the paracentral lobule
Tactile
Fine touch: spinal nerve sensory fibers→spinal ganglion→medial part of posterior root→posterior cord of spinal cord→fascicle gracilis, fasciculus cuneatee
Coarse touch: spinal nerve sensory fibers → spinal ganglion → medial part of the posterior root → nucleus proper of the posterior horn → most of them cross to the contralateral anterior funiculus through the anterior commissure of the white matter, a small part is on the ipsilateral anterior funiculus → anterior spinothalamic tract → in the medulla oblongata The middle and lateral spinothalamic tracts merge to form the spinothalamic tract/spinal lemniscus
Deep sensation: spinal nerve sensory fibers → spinal ganglion → medial part of the posterior root → posterior cord of the spinal cord → fasciculus fasciculata, fasciculus cuneatus → nucleus of fasciculus fasciculata of medulla oblongata, nucleus of cuneate fasciculus → cross to form medial lemniscus → ventroposterolateral thalamus nucleus → thalamocortex Bundle → middle and upper part of postcentral gyrus and posterior part of paracentral lobule
Arrangement of sensory tracts in the spinal cord
Spinothalamic tract (internal → external): cervical, thoracic, lumbar, sacral (same as pyramidal tract); further subdivided, temperature sensation is posterior, pain sensation is in the middle, and touch is in the anterior direction
Thin fasciculus (inner), cuneate fasciculus (external): sacrum, waist, chest, and neck; below T4, the posterior cord has only a thin fasciculus that conducts deep sensation in the lower part of the body, and above T4, a cuneate fasciculus (located in the posterior cord) that conducts deep sensation in the upper part of the body is added Thin bundle outside)
Segmental innervation: C5~C7 on the radial side of the upper limb, C8 and T1 on the ulnar side of the forearm and hand, T2 on the inner side of the upper arm; L1~L3 on the front of the thigh, L4~L5 on the front of the calf, S1~ on the calf and posterior thigh. S2, perianal sellar area is S4~S5
Damage localization
Classification of sensory disorders
Suppressive symptoms
Sensory loss
Total sensory loss: When conscious, there is no feeling at all in a certain part (all senses are lost)
Dissociated sensory loss: When conscious, a certain sensory disorder occurs in a certain part while other sensations in that part are preserved; among them, those with only deep sensory loss and shallow sensory preservation are also called schizotypal sensory disorders.
Reduced sensation
Irritant symptoms
Hyperesthesia: Normally, a stimulus that does not cause discomfort/can only cause a slight sensation to normal people, but the patient feels very strongly or even intolerable; common in superficial sensory disorders
Hyperpathia: Due to the increased stimulation threshold and prolonged reaction time, the stimulation must reach a very strong level before you can feel it; it takes a latency period after stimulation to feel a strong, unclearly located discomfort; the patient cannot point it out correctly The nature and intensity of the stimulation cannot be judged by the location of the stimulation; sometimes you can feel the stimulation point spreading to the surroundings, and there is an "after-effect" (it lasts for a period of time and then disappears)
Paresthesia (paresthesia): refers to the patient feeling ant-like sensation, numbness, itching, heavy pressure, acupuncture, cold and heat, and swelling in certain parts without any external stimulation, but there is no sensory disorder on objective examination; common in peripheral/autonomic neuropathy
Pain
Local pain: localized pain in the local area of the lesion
Radiating pain: When the nerve root/nerve trunk is stimulated by a lesion, the pain may not only appear at the stimulation site, but also spread to other innervated areas along the affected sensory nerve; such as sciatica
Spreading pain: pain spreading to adjacent parts to other branches; such as trigeminal neuralgia
Referred pain: When there is visceral disease, pain may also occur on the surface of the body controlled by the spinal cord segment equivalent to the diseased viscera; for example, in angina pectoris, there may be pain in the left chest and inner side of the left upper limb.
Causalgia: It is a persistent and intense pain like burning in the hands and feet, accompanied by sweating, vasomotion, and delayed dystrophy; it is common in incomplete damage to the median nerve/tibial nerve, and patients often use cold water Soak the affected limb to relieve pain; it is now believed that it may be due to the formation of a pseudosynapse between the sympathetic efferent fibers at the injured site and the unmyelinated C fibers, where the sympathetic efferent impulses are short-circuited, and the impulses are transmitted to the C fibers and then Return to center
Phantom limb pain: feeling that the severed limb still exists after amputation/pain in the stump
Lightening pain: most common in patients with tuberculosis spinal cord; due to involvement of the posterior roots/posterior columns of the thoracic/lumbosacral spinal cord, episodic short-lived electric shock-like severe pain in the lower limbs; occurs when accompanied by damage to the nerves that innervate the internal organs Visceral dysfunction is called a "crisis" (gastric crisis is the most common) and burning pain occurs.
Positioning diagnosis
Peripheral type: symmetrical various sensory disorders at the end of the limbs, with a glove-sock-like distribution, with the distal end being heavier than the proximal end, accompanied by autonomic nervous system dysfunction; such as polyneuropathy
Nerve trunk type: All sensations in the distribution area of a damaged nerve trunk are reduced/disappeared (banded/segmental); such as mononeuropathy
Posterior root type: unilateral segmental sensory disorder (the scope is consistent with the nerve root distribution), often accompanied by severe radiating pain; such as lumbar disc herniation, extramedullary tumors
Spinal type/intramedullary type
Posterior horn type: segmental dissociated sensory disorder on the affected side (impairment of pain and temperature sensation with preservation of touch and deep sensation); seen in syringomyelia and intraspinal tumors
This is because pain and temperature sensations enter the posterior horn, while some tactile and deep sensory fibers directly enter the posterior cord without passing through the posterior horn.
Anterior commissure type: bilateral segmental symmetrical dissociated sensory impairment below the damaged level (impaired pain and temperature sensation with preserved touch and deep sensation); seen in early stages of syringomyelia and intraspinal tumors
Conduction bundle type
Posterior funiculus type: deep sensory and fine tactile impairment below the damaged level, sensory ataxia; seen in diabetes, tuberculosis, and subacute combined degeneration
Lateral cord type: loss of pain and temperature sensation on the contralateral side below the damaged level but preservation of touch and deep sensation (dissociative sensory disorder)
Spinal cord hemidissection type (spinal cord hemisection syndrome)
Transverse spinal cord damage: all sensory impairments below the damaged level, and there may be allergic zones above the level; for example, there may be signs of pyramidal tract damage in the cervicothoracic segment; seen in myelitis and spinal cord tumors
Cona equina type: loss of saddle sensation in the perianal and perineal areas; posterior root type sensory disturbance and severe pain may still occur in cauda equina lesions
Brainstem type
Lesions in the middle part of the medulla oblongata damage the medial lemniscus: there is loss of deep sensation in the contralateral limb but normal pain and temperature sensation (dissociative sensory disorder)
Lesions of the lateral medulla oblongata damage the spinal trigeminal tract nucleus and spinothalamic tract: facial sensory impairment on the affected side and pain and temperature impairment on the contralateral body and limbs (crossed sensory disorder)
Lesions and damage to the pons and midbrain: contralateral facial sensory impairment and partial body deep and superficial sensory impairment
Thalamic type: Complete sensory loss/reduction in the contralateral side of the body (including the face); deep sensory and tactile impairments are more severe, more severe distally, often accompanied by spontaneous pain (thalamic pain)/hyperesthesia/reduction of sensation in the affected limb (thalamic pain) wrong
Internal capsule type: loss/reduction of deep and superficial sensation on the contralateral side of the body, and in severe cases, "triple hemisphere" syndrome may occur
Cortical type: ① Compound sensory impairment on the contralateral side with mild pain and temperature impairment; ② Single-limb sensory impairment may occur when some areas are damaged; ③ Localized sensory epilepsy (ictal paresthesias) may occur due to irritating lesions.
3. Movement system
(1) Cone system
Anatomy and Physiology
upper motor neuron
Composition: large pyramidal cells in the motor area of the precentral gyrus of the frontal lobe①→
①Corticospinal tract → Posterior limb of internal capsule → Middle 3/5 of midbrain cerebral peduncle → Basal part of pons → 85% crosses in the medulla oblongata pyramid to the opposite side to form lateral corticospinal tract, a small part does not cross to form anterior corticospinal tract (but in During the descent, they gradually cross to the opposite side, only a few never cross) → the anterior horn of the spinal cord;
② The cortical brainstem tract → the genu of the internal capsule → crosses to the opposite side at the plane of each cranial nerve nucleus and terminates in each cranial nerve motor nucleus (except for the lower part of the facial nerve nucleus and the hypoglossal nerve nucleus, which are only innervated by the contralateral side, the rest are innervated by both sides) side dominance)
Function: Release and transmit voluntary movements to lower motor neurons, and control and dominate their activities
Injury: produces central paralysis/spastic paralysis; characteristics: ① Central cranial nerve damage only causes paralysis of the contralateral tongue muscle and lower part of the facial muscle; ② Limb paralysis caused by pyramidal tract can manifest as monoplegia, hemiplegia, and paraplegia , quadriplegia, but generally the distal muscles of the limbs are more seriously affected, the extensor muscles of the upper limbs are more serious than the flexor muscles, the external rotators are more serious than the adductor muscles, the hand flexors are more serious than the extensors, and the lower limbs are just the opposite of the upper limbs; ③ muscles Increased tension - the "clasp-knife phenomenon" (when the affected limb is pulled and stretched by an external force, resistance appears at the beginning. When the stretch continues to a certain level, the resistance suddenly disappears and the affected limb is quickly stretched and stretched) ; ④ Tendon hyperreflexia: active, hyperactive, reflex diffusion, clonus; ⑤ Shallow reflex hyporeflexia/disappearance; ⑥ Pathological reflex positive; ⑦ No obvious muscle atrophy
Lower motor neuron/peripheral motor neuron
Composition: spinal cord anterior horn motor neurons/cranial nerve motor nuclei and their axons
Function: combine and transmit nerve impulses to cause muscle contraction
Injury: Produces peripheral paralysis / flaccid paralysis
Differentiation of upper and lower motor neuron paralysis:
Damage localization
Upper motor neuron paralysis - spastic paralysis
Cortical type: Contralateral central monoplegia occurs when localized lesions occur (one upper limb, lower limb, face); irritating lesions can cause localized and paroxysmal convulsions in the corresponding parts of the contralateral limbs
Internal cyst type: typically manifests as "triple deviation" syndrome
Brainstem type: Damage to one side causes cross paralysis (peripheral cranial nerve palsy on the affected side, central paralysis of the contralateral limb), and may be accompanied by hemiplegic sensory impairment on the side of hemiplegia
Spinal type: often accompanied by sensory impairment below the level of damage and urinary and fecal dysfunction
Medullary ~ cervical enlargement: lesions on one side cause spinal hemiplegia (without cranial nerve palsy), and transverse lesions cause central quadriplegia
Neck enlargement: Transverse lesions cause flaccid paralysis of the upper limbs and central paralysis of the lower limbs.
Neck enlargement ~ lumbosacral enlargement: transverse lesions causing spastic paraplegia
Lower lumbosacral segment: flaccid paralysis of the lower limbs
Lower motor neuron paralysis - flaccid paralysis
Anterior horn cells of the spinal cord: only cause segmental flaccid paralysis without sensory impairment; acute onset is more common in poliomyelitis, while slow onset is common in fasciculations and motor neuron disease
Anterior root: only causes segmental flaccid paralysis without sensory impairment; but often damages the posterior root at the same time, causing radicular pain and segmental sensory impairment; more common in extramedullary tumor compression, meningitis or vertebral lesions
Nervous plexus: Involves most nerves in a limb, causing flaccid paralysis, sensory impairment and autonomic nervous system dysfunction, which may be accompanied by pain
Peripheral nerves: flaccid paralysis of the innervating muscles, accompanied by sensory and autonomic nerve dysfunction/pain
(2) Extrapyramidal system
Anatomy and Physiology
Broadly speaking: striatal system, subthalamic nucleus, substantia nigra, red nucleus, reticular formation, thalamus, cerebellar dentate nucleus, vestibular nucleus, medulla oblongata olivary nucleus
Narrow sense - striatal system (basal ganglia): striatum (caudate nucleus lentiform nucleus (putamen globus pallidus)) claustrum amygdala; caudate nucleus putamen = neostriatum; globus pallidus = Old striatum; amygdala claustrum = ancient striatum
Function: Extensively connected with the motor area (Area 4) and premotor area (Area 6) of the cerebral cortex → regulates muscle tone, coordinates skeletal muscle movement, maintains and adjusts posture, and is responsible for semi-automatic stereotyped movements/reflex movements
Injury manifestations
Changes in muscle tone (myotonia): Characterized by strengthening of both extensor and flexor muscles, manifested as lead pipe-like rigidity and gear-like rigidity (see "Parkinson's disease" section)
Involuntary movements: Abnormal and purposeless activities that are not subject to subjective control when the patient is conscious.
Tremor: It is a rhythmic oscillatory movement of a certain part of the human body caused by the alternating contraction of agonist muscles and antagonist muscles.
Physiological tremor: subtle tremor; seen in the elderly
Functional tremor: such as strong physiological tremor, hysterical tremor, etc.
Pathological tremor
Resting tremor: see section on “Parkinson’s disease”
Action tremor
① Postural tremor: It does not appear during voluntary movement. It only appears when the movement is completed and the limbs and trunk are actively maintained in a certain posture. The tremor disappears when the limbs are relaxed and becomes obvious again when the muscles are tense. It is seen in essential tremor and chronic tremor. Alcohol poisoning, hepatic encephalopathy (asterixis), hepatolenticular degeneration, etc.
②Kinematic tremor/intentional tremor: refers to the tremor that occurs during movement when the limbs are purposefully approaching a target; the closer the target is, the more obvious the tremor is; when the target is reached and the posture is maintained, the tremor can sometimes still occur. Persistent; seen in cerebellar lesions, thalamic/red nucleus lesions
Choreic movement: manifested as involuntary movements of the limbs that are irregular, unrhythmic, aimless, asymmetrical, rapid and changeable, with varying amplitudes of movement - shrugging the shoulders, turning the neck, stretching the arms, raising the arms, waving the hands , extension and flexion of fingers; the upper limbs are heavier, and the distal end is heavier, aggravated by random movements/emotional excitement, and disappear after falling asleep; movements such as winking, winking, pouting, and tongue extension may occur on the head and face; in severe cases, the limbs may have large and frequent movements; seen in chorea, HD
Athetosis/finger paddling/mobile spasm: manifested as increased/lowered migratory muscle tone in the distal limbs → intermittent slow alternating extension and flexion of fingers/toes (worm crawling) (like); sometimes unclear pronunciation and grimacing; seen in striatal calcification, kernicterus, and hepatolenticular degeneration
Torsion spasm/dystonia muasulorum deformans: manifested by slow involuntary torsional/spiral rotational movements around the long axis of the trunk/limb; spasmodic torticollis that occurs when cervical muscles are involved Is a special localized type; seen in primary genetic diseases, hepatolenticular degeneration, drug reactions (such as phenothiazines)
Hemiballismus: manifested as violent throwing-like involuntary movement of one limb, with large amplitude and strong force, focusing on the proximal end of the limb; seen in damage to the contralateral subthalamic nucleus, striatum and subthalamus Nuclear conduction pathway lesions
Tic syndrome (tic): manifested as rapid contraction of single/multiple muscles, fixed in one place or wandering, manifested as winking, facial muscle twitching, nose flaring, pouting, shrugging, and turning the neck; when breathing is involved and pronunciation muscles, twitching may be accompanied by involuntary pronunciation or Tourette syndrome (tourette syndrome); spontaneous abnormal muscle movements of the mouth, cheeks, tongue, eyelids and other muscles after middle age are called Meige's disease; seen in basal ganglia lesions/ Mental factors (mostly habitual actions), drug factors (acute dystonia, tardive dyskinesia)
Attachment: Key points in the differential diagnosis of pyramidal and extrapyramidal syndromes
(3) Cerebellar system
Anatomy and Physiology
structure
Surface: Pompotule leaf, anterior leaf, posterior leaf
Inside: cerebellar cortex and cerebellar medulla (containing the fastigial nucleus, globular nucleus, plugate nucleus and dentate nucleus arranged from inside to outside)
Genesis
Protocerebellum/archaeocerebellum (flocculus nodular lobe, parietal lobe): receives impulses from the vestibular organ; closely related to body balance
Old cerebellum (the lumbrical cones and uvula of the anterior lobe and posterior lobe): receives proprioception from the spinal cord; maintains body posture and regulates muscle tone
New cerebellum (posterior lobe except vermis and vermis): develops at the same time as the cerebral hemispheres; coordinates voluntary movements
Fiber and its connections
Afferent fibers: spinocerebellar tract, vestibulocerebellar tract, pontocerebellar tract, olivocerebellar tract
Efferent fibers
Dentate nucleus-red nucleus-spinal tract: dentate nucleus → crosses to the contralateral red nucleus (Wernkink’s cross) → crosses to the ipsilateral anterior horn of the spinal cord (Forel’s cross); regulates movement
Dentate nucleus-red nucleus-thalamic tract: regulates the pyramidal system and extrapyramidal system
Typical spinal cord tract: reticulospinal tract/vestibulospinal tract → regulate movement; vestibular nucleus, medial longitudinal fasciculus → regulate eye movement
Function: Maintain body balance, control posture and gait, regulate muscle tension, and coordinate voluntary movements
Damage localization
(One side) Cerebellar hemisphere damage
Characteristics: Ipsilateral limb ataxia (the upper limb is heavier than the lower limb, the distal end is heavier than the proximal end, and fine movements are heavier than gross movements), often with motor tremor, hypotonia, and nystagmus (especially the eyes looking toward the affected side) ), cerebellar speech may occur
Ataxia: refers to clumsiness and uncoordinated movements caused by cerebellar, proprioceptive and vestibular dysfunction
Cerebellar
Abnormal posture and gait: unsteady standing, staggering gait, legs apart when walking, limbs abducted when sitting
Voluntary movement coordination disorder: Movements tend to exceed the target (inadequate estimation of the distance, speed, and strength of movement → dysmetria → incorrect finger-nose test, heel-knee-shin test, alternating movements, etc.); intention tremor
Dysarthria: Slow speech, unclear pronunciation, intermittent/frustrated voice (telegraphic/explosive/poetry-like speech)
Ocular movement disorder: Large nystagmus in both eyes, and in a few cases, downbeat nystagmus, rebound nystagmus, and skew deviation may occur.
Dissociative strabismus: The ipsilateral eyeball is downward and inward, while the contralateral eyeball is upward and outward. It may be the result of damage to the cerebellum and other central connections.
Hypotonia: When the patient takes a sitting position, the legs naturally droop. After percussion tendon reflex, the calf keeps swinging like a pendulum (pendulum-like tendon reflex); a combined flexion sign may also occur (see below)
Cerebral: Lesions in one side of the brain cause ataxia in the contralateral limbs; symptoms are mild, accompanied by symptoms in respective brain regions (divided into frontal lobe, temporal lobe, parietal lobe, and occipital lobe)
Sensory: Deep sensory impairment prevents patients from distinguishing the position and direction of movement of limbs; most common in damage to the posterior cord of the spinal cord; manifested by unsteady standing, uncontrollable step distance, and a feeling of stepping on cotton; symptoms are mild and dark when the eyes are opened / Symptoms worsen when eyes are closed (it is difficult to detect positive signs with eyes closed); no dizziness, nystagmus, or speech impairment
Vestibular: unstable standing, changing head position can aggravate symptoms, leaning to the affected side when walking, accompanied by obvious dizziness, nausea and vomiting, and nystagmus; coordinated movement of limbs and speech function are normal
Damage to the cerebellar vermis: ① Axial balance disorder/truncal ataxia: the trunk cannot maintain an upright posture, is unstable when standing, has a positive sign of difficulty standing with eyes closed (opening eyes does not improve); feet apart when walking, staggering, drunkenness ② Limb ataxia and nystagmus are not obvious, muscle tone is normal, and speech disorder is obvious
Cerebellar seizure: When a space-occupying lesion in the cerebellum compresses the brainstem, paroxysmal tonic convulsions may occur, or a state of cerebral tonicity may occur, manifesting as rigidity of the limbs, opisthotonus, and confusion.
Chronic diffuse damage to the cerebellum: limb ataxia is not obvious (∵ compensatory effect of the new cerebellum)
Cognitive impairment: affective cerebellar syndrome