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*Only for medical professionals' reference to read clinical practical dry goods sharing.
Peripheral neuropathy refers to the structure and dysfunction of peripheral motor, sensory and autonomic nerves.
Different diameters and types of nerve fibers can cause different neuropathy.
Then, how to make a standardized diagnosis of peripheral neuropathy, and what is the clinical thinking? Let’s sort it out with everyone today! Anatomy of peripheral nerves Peripheral nerves include cranial nerves and spinal nerves other than the olfactory and optic nerves.
Cranial nerve: the cranial nerve that originates from the ventrolateral side of the brainstem.
Spinal nerves: All nerve structures located outside the papilla of the spinal cord and brainstem, which originate from the ventral and dorsal sides of the spinal cord.
Figure 1: Schematic diagram of cranial nerves and spinal nerves.
Significance of clinical manifestations.
Peripheral nerves are composed of motor, sensory and autonomic nerves.
Each peripheral nerve contains different types and numbers of nerve fibers, so motor, sensory, and autonomic functions can occur.
One or more clinical symptoms such as temperature and reflex disorders.
For peripheral neuropathy, we must first ask the patient's onset process and past medical history in detail, and then perform a detailed physical examination on this basis to make a preliminary judgment on the diagnosis.
1 Sensory changes of the affected nerve: Most patients with acute or chronic inflammatory demyelinating polyradiculopathy and toxic neuropathy have sensory symptoms.
Numbness, swelling, or more sensitive to painful stimuli, physical examination can reveal gloves and sock-like changes in length-dependent peripheral neuropathy, which gradually develop proximally.
Motor changes: The lack of symptoms is manifested as a single decrease and loss of muscle strength, and can also be combined with other sensory neuropathies.
The main symptoms of irritation are muscle tremor.
Autonomic nerve function changes: it can be manifested as sweating, vascular dyskinesia, digestive system and urinary system abnormalities, which often occur with sensory nerve damage, and rarely with motor nerve damage.
2 The location of the lesion is to determine whether the lesion is located in the nerve root, nerve trunk or nerve ending longitudinally.
Determine the mononeuropathy, multiple mononeuropathy, plexopathy or multiple peripheral neuropathy in the horizontal direction.
3 Development law Most immune-mediated or infectious neurological diseases have a clear onset date.
Uncertain dates of onset often indicate toxic, metabolic, hereditary or idiopathic causes.
4 The nature of the disease analyzes the unique clinical background of the patient, and a comprehensive understanding of the patient's past history, medication history, personal history, family history and related systems, especially family history, can often find clues to the diagnosis of the disease.
When analyzing the clinical data of patients, we must first consider the causes of common peripheral neuropathies, and actively search for clinical clues to these causes.
Table 1 and Table 2 are the common causes of hereditary peripheral neuropathy and acquired peripheral neuropathy, respectively.
Table 1: The etiology of hereditary peripheral neuropathy Table 2: The etiology and pathological changes of acquired peripheral neuropathy cannot be ignored.
Pathological examination is an important means to verify whether the clinical classification of peripheral neuropathy is correct.
When peripheral nerves are damaged, they are mainly manifested in four pathological forms, namely Waller degeneration, axon degeneration, neuronal degeneration, and segmental demyelination.
Diseases of different structures often appear mixed, but the degree of change varies in each disease.
Wallerian degeneration: common in trauma; axonal degeneration: common in toxic metabolic and dystrophic; neuronal degeneration: common in cancerous sensory neuron disease, mercury poisoning; segmental demyelination: common in inflammatory, Heredity, toxicity, metabolic disorder.
Pathological changes should not be ignored Figure 2: Schematic diagram of the pathological form of peripheral neuropathy Targeted auxiliary examination laboratory examinations: including blood routine, erythrocyte sedimentation rate, blood sugar, liver function, thyroid function, creatine kinase, vitamin B12 level, protein electrophoresis, anti-neutrality Granulocyte cytoplasmic antibody, antinuclear antibody, consider special genetic testing for hereditary neuropathy.
Cerebrospinal fluid examination: For peripheral neuropathy involving nerve roots, an increase in cerebrospinal fluid protein can often be found.
For diseases that mainly damage the distal peripheral nerves, the cerebrospinal fluid is generally not abnormal. Electrophysiological examination: Electrophysiological examination helps to determine whether there is peripheral nerve damage and the extent and distribution of damage.
Generally, axonal damage is manifested as a normal or low nerve conduction velocity, and the amplitude of the action potential is reduced; myelin damage is manifested as a significant slowdown of the nerve conduction velocity, while the amplitude of the action potential is not significantly changed.
Pathological examination: The routine sampling site is the sural nerve.
Pay attention to the degree of damage to the myelin sheath and axon of the myelinated nerve fibers of the peripheral nerve.
Genetic testing: Almost all hereditary peripheral neuropathies are inherited by a single gene.
After the diagnosis is confirmed through genetic testing, the clinical, electrophysiological and pathological characteristics of the disease can be understood in turn, and the understanding of the disease can be improved.
Figure 3: Summary of ideas for auxiliary examination of peripheral neuropathy: The diagnostic ideas for patients with peripheral neuropathy include: 1.
Detailed medical history, including current medical history, past history, and family history of at least one generation; 2.
Differentiate and analyze the collected data to find induction Factors; 3.
Choose targeted auxiliary examinations for comprehensive diagnosis.
Reference: [1]Crone C et al.
Diagnosis of acute neuropathies.
J Neurol,2007,254:1151-1169.
[2]Strand NH,et al.
Mechanism of Action of Peripheral Nerve Stimulation.
Curr Pain Headache Rep 2021 May 11;25(7).
[3] Zhou Shuxin, etc.
, Peripheral Neuropathy: Differential Diagnosis and Management.
[J] Chinese Journal of General Medicine, 2010.
12(13)12A.
[4] Wu Jiang, "Neurology" (eight-year system) , Second Edition), People's Medical Publishing House.
[5] "Difficult Nerve Cases" edited by Qi Xiaokun, People's Medical Publishing House.
Peripheral neuropathy refers to the structure and dysfunction of peripheral motor, sensory and autonomic nerves.
Different diameters and types of nerve fibers can cause different neuropathy.
Then, how to make a standardized diagnosis of peripheral neuropathy, and what is the clinical thinking? Let’s sort it out with everyone today! Anatomy of peripheral nerves Peripheral nerves include cranial nerves and spinal nerves other than the olfactory and optic nerves.
Cranial nerve: the cranial nerve that originates from the ventrolateral side of the brainstem.
Spinal nerves: All nerve structures located outside the papilla of the spinal cord and brainstem, which originate from the ventral and dorsal sides of the spinal cord.
Figure 1: Schematic diagram of cranial nerves and spinal nerves.
Significance of clinical manifestations.
Peripheral nerves are composed of motor, sensory and autonomic nerves.
Each peripheral nerve contains different types and numbers of nerve fibers, so motor, sensory, and autonomic functions can occur.
One or more clinical symptoms such as temperature and reflex disorders.
For peripheral neuropathy, we must first ask the patient's onset process and past medical history in detail, and then perform a detailed physical examination on this basis to make a preliminary judgment on the diagnosis.
1 Sensory changes of the affected nerve: Most patients with acute or chronic inflammatory demyelinating polyradiculopathy and toxic neuropathy have sensory symptoms.
Numbness, swelling, or more sensitive to painful stimuli, physical examination can reveal gloves and sock-like changes in length-dependent peripheral neuropathy, which gradually develop proximally.
Motor changes: The lack of symptoms is manifested as a single decrease and loss of muscle strength, and can also be combined with other sensory neuropathies.
The main symptoms of irritation are muscle tremor.
Autonomic nerve function changes: it can be manifested as sweating, vascular dyskinesia, digestive system and urinary system abnormalities, which often occur with sensory nerve damage, and rarely with motor nerve damage.
2 The location of the lesion is to determine whether the lesion is located in the nerve root, nerve trunk or nerve ending longitudinally.
Determine the mononeuropathy, multiple mononeuropathy, plexopathy or multiple peripheral neuropathy in the horizontal direction.
3 Development law Most immune-mediated or infectious neurological diseases have a clear onset date.
Uncertain dates of onset often indicate toxic, metabolic, hereditary or idiopathic causes.
4 The nature of the disease analyzes the unique clinical background of the patient, and a comprehensive understanding of the patient's past history, medication history, personal history, family history and related systems, especially family history, can often find clues to the diagnosis of the disease.
When analyzing the clinical data of patients, we must first consider the causes of common peripheral neuropathies, and actively search for clinical clues to these causes.
Table 1 and Table 2 are the common causes of hereditary peripheral neuropathy and acquired peripheral neuropathy, respectively.
Table 1: The etiology of hereditary peripheral neuropathy Table 2: The etiology and pathological changes of acquired peripheral neuropathy cannot be ignored.
Pathological examination is an important means to verify whether the clinical classification of peripheral neuropathy is correct.
When peripheral nerves are damaged, they are mainly manifested in four pathological forms, namely Waller degeneration, axon degeneration, neuronal degeneration, and segmental demyelination.
Diseases of different structures often appear mixed, but the degree of change varies in each disease.
Wallerian degeneration: common in trauma; axonal degeneration: common in toxic metabolic and dystrophic; neuronal degeneration: common in cancerous sensory neuron disease, mercury poisoning; segmental demyelination: common in inflammatory, Heredity, toxicity, metabolic disorder.
Pathological changes should not be ignored Figure 2: Schematic diagram of the pathological form of peripheral neuropathy Targeted auxiliary examination laboratory examinations: including blood routine, erythrocyte sedimentation rate, blood sugar, liver function, thyroid function, creatine kinase, vitamin B12 level, protein electrophoresis, anti-neutrality Granulocyte cytoplasmic antibody, antinuclear antibody, consider special genetic testing for hereditary neuropathy.
Cerebrospinal fluid examination: For peripheral neuropathy involving nerve roots, an increase in cerebrospinal fluid protein can often be found.
For diseases that mainly damage the distal peripheral nerves, the cerebrospinal fluid is generally not abnormal. Electrophysiological examination: Electrophysiological examination helps to determine whether there is peripheral nerve damage and the extent and distribution of damage.
Generally, axonal damage is manifested as a normal or low nerve conduction velocity, and the amplitude of the action potential is reduced; myelin damage is manifested as a significant slowdown of the nerve conduction velocity, while the amplitude of the action potential is not significantly changed.
Pathological examination: The routine sampling site is the sural nerve.
Pay attention to the degree of damage to the myelin sheath and axon of the myelinated nerve fibers of the peripheral nerve.
Genetic testing: Almost all hereditary peripheral neuropathies are inherited by a single gene.
After the diagnosis is confirmed through genetic testing, the clinical, electrophysiological and pathological characteristics of the disease can be understood in turn, and the understanding of the disease can be improved.
Figure 3: Summary of ideas for auxiliary examination of peripheral neuropathy: The diagnostic ideas for patients with peripheral neuropathy include: 1.
Detailed medical history, including current medical history, past history, and family history of at least one generation; 2.
Differentiate and analyze the collected data to find induction Factors; 3.
Choose targeted auxiliary examinations for comprehensive diagnosis.
Reference: [1]Crone C et al.
Diagnosis of acute neuropathies.
J Neurol,2007,254:1151-1169.
[2]Strand NH,et al.
Mechanism of Action of Peripheral Nerve Stimulation.
Curr Pain Headache Rep 2021 May 11;25(7).
[3] Zhou Shuxin, etc.
, Peripheral Neuropathy: Differential Diagnosis and Management.
[J] Chinese Journal of General Medicine, 2010.
12(13)12A.
[4] Wu Jiang, "Neurology" (eight-year system) , Second Edition), People's Medical Publishing House.
[5] "Difficult Nerve Cases" edited by Qi Xiaokun, People's Medical Publishing House.