Charcot-Marie-Tooth disease, also known as hereditary sensory and motor neuropathy, is a group of inherited peripheral neuropathies that affect the nerves responsible for muscle movement and sensation. It was first described by Jean-Martin Charcot, Pierre Marie, and Howard Henry Tooth in the late 19th century.
CMT is a common neurological disorder, with a prevalence estimated to be 1 in 2,500 individuals. It affects in both males and females and can present in childhood or adulthood. CMT is typically inherited in an autosomal dominant pattern, although autosomal recessive and X-linked inheritance patterns are also observed.
The disease is characterized by progressive muscle weakness and wasting, particularly in the distal extremities such as the feet and hands. Sensory loss, including decreased touch, temperature, and vibration sensation, is also common. These symptoms can lead to difficulties with walking, balance, and fine motor skills.
The underlying cause of CMT is genetic mutations that affect the structure or function of peripheral nerves. Over 100 different genes have been associated with CMT, each with its specific pattern of inheritance and clinical features. These genetic mutations disrupt the normal production of proteins in the structure and function of peripheral nerves, leading to nerve degeneration and dysfunction.
Epidemiology
Prevalence: The prevalence of CMT is estimated to be around 1 in 2,500 individuals, making it common. However, the prevalence may vary among different populations and ethnicities.
Inheritance Patterns: CMT can be inherited in different patterns, including autosomal dominant, autosomal recessive, and X-linked inheritance. The prevalence of each inheritance pattern may vary for different subtypes of CMT.
Age of Onset: Some subtypes of CMT present in childhood or adolescence, while others may have a later onset in adulthood.
Geographic Distribution: CMT occurs worldwide, and its prevalence may vary across different regions and populations. Certain subtypes of CMT may be more common in specific ethnic groups.
Subtypes: CMT is a heterogeneous disorder with multiple subtypes, each associated with specific genetic mutations. The prevalence of different CMT subtypes may vary among populations.
Anatomy
Pathophysiology
Nerve Fiber Abnormalities: CMT affects the peripheral nerves, which are responsible for transmitting signals between the CNS and the rest of the body.
Myelin Sheath Dysfunction: In some forms of CMT, the mutations affect genes which are important for the production and maintenance of myelin sheath, a protective covering around the nerve fibers. Myelin sheath abnormalities can lead to slowed nerve conduction and impaired signal transmission.
Axonal Degeneration: In other forms of CMT, the mutations primarily affect the axons themselves, which are the long extensions of nerve cells. Axonal degeneration can lead to progressive loss of nerve function and muscle weakness.
Impaired Nerve Regeneration: In addition to the primary abnormalities in the nerve fibers, CMT can also involve impaired nerve regeneration. The damaged nerves may have a reduced capacity to regenerate and repair themselves.
Etiology
Genetic Mutations: The primary etiology of CMT are genetic mutations. CMT is a genetically heterogeneous disorder, meaning it can be caused by mutations of different genes. Several genes have been associated with different subtypes of CMT, including PMP22, MPZ, GJB1, MFN2, and others.
Inheritance Patterns: CMT can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific gene involved. Some forms of CMT result from spontaneous genetic mutations with no family history.
Gene Function: The genes associated with CMT are involved in the structure and function of peripheral nerves. Mutations in these genes disrupt normal nerve development, myelin production, or axonal integrity, leading to the characteristic features of CMT.
Genetic Variability: The wide genetic variability in CMT results in variations in the clinical presentation and severity of the disease. Different gene mutations can affect different aspects of nerve function, leading to variability in symptoms and disease progression.
Genetics
Prognostic Factors
Genetic Subtype: The specific genetic subtype of CMT can influence the prognosis. Some subtypes may have a milder course with slower disease progression, while others may lead to more severe symptoms and faster disease progression.
Disease Severity at Diagnosis: The severity of symptoms and functional impairment can provide insights into the prognosis. Individuals with more severe initial symptoms may have a higher risk of disability and faster disease progression.
Electrophysiological Findings: Electrophysiological studies, such as nerve conduction studies and electromyography, can help assess the extent of nerve damage and demyelination. Severe electrophysiological abnormalities may indicate a worse prognosis.
Disease Progression Rate: The rate at which the disease progresses can vary among individuals with CMT. Faster disease progression may indicate a poorer prognosis.
Comorbidities: The presence of additional medical conditions or comorbidities can impact the overall prognosis and functional outcomes in individuals with CMT.
Clinical History
CLINICAL HISTORY
Age group:
CMT can present at any age, from early childhood to late adulthood.
The age of onset may vary depending on the specific subtype of CMT.
Some subtypes may have an early onset, while others may present later in life.
Physical Examination
PHYSICAL EXAMINATION
Motor Examination:
Muscle weakness: Assess the strength of various muscle groups, especially in the lower limbs, such as hip flexors, knee extensors, ankle dorsiflexors, and toe extensors.
Muscle atrophy: Look for signs of muscle wasting, particularly in the lower legs and feet.
Foot deformities: Examine for high arches (pes cavus), hammer toes, or claw-like deformities.
Hand weakness: Assess grip strength and fine motor dexterity.
Sensory Examination:
Evaluate sensory function, including light touch, vibration sense, and proprioception, in the distal extremities.
Test for diminished or absent sensation, particularly in the feet and hands.
Reflexes:
Check deep tendon reflexes, such as the patellar reflex (knee jerk) and ankle reflex (Achilles reflex).
Look for signs of hyperreflexia or reduced reflexes.
Gait Assessment:
Observe the patient’s gait, noting any abnormalities such as foot drop, high stepping, or frequent tripping.
Assess balance and coordination during walking, turning, and other motor tasks.
Other Findings:
Evaluate the presence of associated features, such as scoliosis (spine curvature), pes planus (flat feet), or pes cavovarus (combination of high arches and inversion of the heel).
Age group
Associated comorbidity
Associated Comorbidity or Activity:
Foot deformities: Many individuals with CMT develop foot deformities such as high arches (pes cavus) or flat feet.
Hand weakness: Weakness and muscle wasting in the hands may be present, affecting fine motor skills.
Sensory changes: Some individuals may experience sensory symptoms such as numbness, tingling, or decreased sensation in the extremities.
Balance and coordination issues: Problems with balance and coordination, leading to frequent tripping or difficulty walking on uneven surfaces.
Muscle weakness and atrophy: Weakness and wasting of the muscles, particularly in the lower legs, may be evident.
Associated activity
Acuity of presentation
Acuity of Presentation:
CMT typically presents gradually and progresses slowly over time.
The rate of disease progression can vary among individuals, even within the same subtype of CMT.
Symptoms may start with mild weakness or sensory changes and progress to more pronounced muscle weakness and functional impairment.
Differential Diagnoses
DIFFERENTIAL DIAGNOSIS
Hereditary Neuropathies:
Hereditary motor and sensory neuropathy type I, II, III, IV, or X.
Distal hereditary motor neuropathies (DHUN)
Hereditary sensory and autonomic neuropathies (HSAN)
Physical therapy and rehabilitation to improve strength, balance, and mobility
Assistive devices such as orthopedic footwear, ankle-foot orthoses (AFOs), braces, or canes to aid in walking and prevent falls.
Occupational therapy to assist daily activities and adaptive strategies.
Administration of Pharmaceutical Agents:
Pain management with nonsteroidal anti-inflammatory drugs (NSAIDs) or other analgesics for neuropathic pain.
Medications to manage associated symptoms such as muscle cramps, muscle spasticity, or bladder dysfunction.
Interventional Procedures:
Surgical correction of foot deformities (e.g., pes cavus) to improve gait and prevent foot ulcers.
Nerve decompression surgery to relieve pressure on compressed nerves.
Tendon transfers or lengthening procedures to correct muscle imbalances and improve function.
Phase of Management:
Regular monitoring of disease progression and functional status.
Adjustment of treatment approaches as needed based on symptoms and functional limitations.
Ongoing collaboration with a multidisciplinary team including neurologists, physical therapists, occupational therapists, orthopedic surgeons, and genetic counsellors.
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References
Charcot-Marie-Tooth Disease Madhu Nagappa; Shivani Sharma; Arun B Taly.ncbi.nlm.nih.gov
Charcot-Marie-Tooth disease, also known as hereditary sensory and motor neuropathy, is a group of inherited peripheral neuropathies that affect the nerves responsible for muscle movement and sensation. It was first described by Jean-Martin Charcot, Pierre Marie, and Howard Henry Tooth in the late 19th century.
CMT is a common neurological disorder, with a prevalence estimated to be 1 in 2,500 individuals. It affects in both males and females and can present in childhood or adulthood. CMT is typically inherited in an autosomal dominant pattern, although autosomal recessive and X-linked inheritance patterns are also observed.
The disease is characterized by progressive muscle weakness and wasting, particularly in the distal extremities such as the feet and hands. Sensory loss, including decreased touch, temperature, and vibration sensation, is also common. These symptoms can lead to difficulties with walking, balance, and fine motor skills.
The underlying cause of CMT is genetic mutations that affect the structure or function of peripheral nerves. Over 100 different genes have been associated with CMT, each with its specific pattern of inheritance and clinical features. These genetic mutations disrupt the normal production of proteins in the structure and function of peripheral nerves, leading to nerve degeneration and dysfunction.
Prevalence: The prevalence of CMT is estimated to be around 1 in 2,500 individuals, making it common. However, the prevalence may vary among different populations and ethnicities.
Inheritance Patterns: CMT can be inherited in different patterns, including autosomal dominant, autosomal recessive, and X-linked inheritance. The prevalence of each inheritance pattern may vary for different subtypes of CMT.
Age of Onset: Some subtypes of CMT present in childhood or adolescence, while others may have a later onset in adulthood.
Geographic Distribution: CMT occurs worldwide, and its prevalence may vary across different regions and populations. Certain subtypes of CMT may be more common in specific ethnic groups.
Subtypes: CMT is a heterogeneous disorder with multiple subtypes, each associated with specific genetic mutations. The prevalence of different CMT subtypes may vary among populations.
Nerve Fiber Abnormalities: CMT affects the peripheral nerves, which are responsible for transmitting signals between the CNS and the rest of the body.
Myelin Sheath Dysfunction: In some forms of CMT, the mutations affect genes which are important for the production and maintenance of myelin sheath, a protective covering around the nerve fibers. Myelin sheath abnormalities can lead to slowed nerve conduction and impaired signal transmission.
Axonal Degeneration: In other forms of CMT, the mutations primarily affect the axons themselves, which are the long extensions of nerve cells. Axonal degeneration can lead to progressive loss of nerve function and muscle weakness.
Impaired Nerve Regeneration: In addition to the primary abnormalities in the nerve fibers, CMT can also involve impaired nerve regeneration. The damaged nerves may have a reduced capacity to regenerate and repair themselves.
Genetic Mutations: The primary etiology of CMT are genetic mutations. CMT is a genetically heterogeneous disorder, meaning it can be caused by mutations of different genes. Several genes have been associated with different subtypes of CMT, including PMP22, MPZ, GJB1, MFN2, and others.
Inheritance Patterns: CMT can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific gene involved. Some forms of CMT result from spontaneous genetic mutations with no family history.
Gene Function: The genes associated with CMT are involved in the structure and function of peripheral nerves. Mutations in these genes disrupt normal nerve development, myelin production, or axonal integrity, leading to the characteristic features of CMT.
Genetic Variability: The wide genetic variability in CMT results in variations in the clinical presentation and severity of the disease. Different gene mutations can affect different aspects of nerve function, leading to variability in symptoms and disease progression.
Genetic Subtype: The specific genetic subtype of CMT can influence the prognosis. Some subtypes may have a milder course with slower disease progression, while others may lead to more severe symptoms and faster disease progression.
Disease Severity at Diagnosis: The severity of symptoms and functional impairment can provide insights into the prognosis. Individuals with more severe initial symptoms may have a higher risk of disability and faster disease progression.
Electrophysiological Findings: Electrophysiological studies, such as nerve conduction studies and electromyography, can help assess the extent of nerve damage and demyelination. Severe electrophysiological abnormalities may indicate a worse prognosis.
Disease Progression Rate: The rate at which the disease progresses can vary among individuals with CMT. Faster disease progression may indicate a poorer prognosis.
Comorbidities: The presence of additional medical conditions or comorbidities can impact the overall prognosis and functional outcomes in individuals with CMT.
CLINICAL HISTORY
Age group:
CMT can present at any age, from early childhood to late adulthood.
The age of onset may vary depending on the specific subtype of CMT.
Some subtypes may have an early onset, while others may present later in life.
PHYSICAL EXAMINATION
Motor Examination:
Muscle weakness: Assess the strength of various muscle groups, especially in the lower limbs, such as hip flexors, knee extensors, ankle dorsiflexors, and toe extensors.
Muscle atrophy: Look for signs of muscle wasting, particularly in the lower legs and feet.
Foot deformities: Examine for high arches (pes cavus), hammer toes, or claw-like deformities.
Hand weakness: Assess grip strength and fine motor dexterity.
Sensory Examination:
Evaluate sensory function, including light touch, vibration sense, and proprioception, in the distal extremities.
Test for diminished or absent sensation, particularly in the feet and hands.
Reflexes:
Check deep tendon reflexes, such as the patellar reflex (knee jerk) and ankle reflex (Achilles reflex).
Look for signs of hyperreflexia or reduced reflexes.
Gait Assessment:
Observe the patient’s gait, noting any abnormalities such as foot drop, high stepping, or frequent tripping.
Assess balance and coordination during walking, turning, and other motor tasks.
Other Findings:
Evaluate the presence of associated features, such as scoliosis (spine curvature), pes planus (flat feet), or pes cavovarus (combination of high arches and inversion of the heel).
Associated Comorbidity or Activity:
Foot deformities: Many individuals with CMT develop foot deformities such as high arches (pes cavus) or flat feet.
Hand weakness: Weakness and muscle wasting in the hands may be present, affecting fine motor skills.
Sensory changes: Some individuals may experience sensory symptoms such as numbness, tingling, or decreased sensation in the extremities.
Balance and coordination issues: Problems with balance and coordination, leading to frequent tripping or difficulty walking on uneven surfaces.
Muscle weakness and atrophy: Weakness and wasting of the muscles, particularly in the lower legs, may be evident.
Acuity of Presentation:
CMT typically presents gradually and progresses slowly over time.
The rate of disease progression can vary among individuals, even within the same subtype of CMT.
Symptoms may start with mild weakness or sensory changes and progress to more pronounced muscle weakness and functional impairment.
DIFFERENTIAL DIAGNOSIS
Hereditary Neuropathies:
Hereditary motor and sensory neuropathy type I, II, III, IV, or X.
Distal hereditary motor neuropathies (DHUN)
Hereditary sensory and autonomic neuropathies (HSAN)
Physical therapy and rehabilitation to improve strength, balance, and mobility
Assistive devices such as orthopedic footwear, ankle-foot orthoses (AFOs), braces, or canes to aid in walking and prevent falls.
Occupational therapy to assist daily activities and adaptive strategies.
Administration of Pharmaceutical Agents:
Pain management with nonsteroidal anti-inflammatory drugs (NSAIDs) or other analgesics for neuropathic pain.
Medications to manage associated symptoms such as muscle cramps, muscle spasticity, or bladder dysfunction.
Interventional Procedures:
Surgical correction of foot deformities (e.g., pes cavus) to improve gait and prevent foot ulcers.
Nerve decompression surgery to relieve pressure on compressed nerves.
Tendon transfers or lengthening procedures to correct muscle imbalances and improve function.
Phase of Management:
Regular monitoring of disease progression and functional status.
Adjustment of treatment approaches as needed based on symptoms and functional limitations.
Ongoing collaboration with a multidisciplinary team including neurologists, physical therapists, occupational therapists, orthopedic surgeons, and genetic counsellors.
Charcot-Marie-Tooth Disease Madhu Nagappa; Shivani Sharma; Arun B Taly.ncbi.nlm.nih.gov
medtigo
Charcot-Marie-Tooth disease
Updated :
July 21, 2023
Charcot-Marie-Tooth disease, also known as hereditary sensory and motor neuropathy, is a group of inherited peripheral neuropathies that affect the nerves responsible for muscle movement and sensation. It was first described by Jean-Martin Charcot, Pierre Marie, and Howard Henry Tooth in the late 19th century.
CMT is a common neurological disorder, with a prevalence estimated to be 1 in 2,500 individuals. It affects in both males and females and can present in childhood or adulthood. CMT is typically inherited in an autosomal dominant pattern, although autosomal recessive and X-linked inheritance patterns are also observed.
The disease is characterized by progressive muscle weakness and wasting, particularly in the distal extremities such as the feet and hands. Sensory loss, including decreased touch, temperature, and vibration sensation, is also common. These symptoms can lead to difficulties with walking, balance, and fine motor skills.
The underlying cause of CMT is genetic mutations that affect the structure or function of peripheral nerves. Over 100 different genes have been associated with CMT, each with its specific pattern of inheritance and clinical features. These genetic mutations disrupt the normal production of proteins in the structure and function of peripheral nerves, leading to nerve degeneration and dysfunction.
Prevalence: The prevalence of CMT is estimated to be around 1 in 2,500 individuals, making it common. However, the prevalence may vary among different populations and ethnicities.
Inheritance Patterns: CMT can be inherited in different patterns, including autosomal dominant, autosomal recessive, and X-linked inheritance. The prevalence of each inheritance pattern may vary for different subtypes of CMT.
Age of Onset: Some subtypes of CMT present in childhood or adolescence, while others may have a later onset in adulthood.
Geographic Distribution: CMT occurs worldwide, and its prevalence may vary across different regions and populations. Certain subtypes of CMT may be more common in specific ethnic groups.
Subtypes: CMT is a heterogeneous disorder with multiple subtypes, each associated with specific genetic mutations. The prevalence of different CMT subtypes may vary among populations.
Nerve Fiber Abnormalities: CMT affects the peripheral nerves, which are responsible for transmitting signals between the CNS and the rest of the body.
Myelin Sheath Dysfunction: In some forms of CMT, the mutations affect genes which are important for the production and maintenance of myelin sheath, a protective covering around the nerve fibers. Myelin sheath abnormalities can lead to slowed nerve conduction and impaired signal transmission.
Axonal Degeneration: In other forms of CMT, the mutations primarily affect the axons themselves, which are the long extensions of nerve cells. Axonal degeneration can lead to progressive loss of nerve function and muscle weakness.
Impaired Nerve Regeneration: In addition to the primary abnormalities in the nerve fibers, CMT can also involve impaired nerve regeneration. The damaged nerves may have a reduced capacity to regenerate and repair themselves.
Genetic Mutations: The primary etiology of CMT are genetic mutations. CMT is a genetically heterogeneous disorder, meaning it can be caused by mutations of different genes. Several genes have been associated with different subtypes of CMT, including PMP22, MPZ, GJB1, MFN2, and others.
Inheritance Patterns: CMT can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific gene involved. Some forms of CMT result from spontaneous genetic mutations with no family history.
Gene Function: The genes associated with CMT are involved in the structure and function of peripheral nerves. Mutations in these genes disrupt normal nerve development, myelin production, or axonal integrity, leading to the characteristic features of CMT.
Genetic Variability: The wide genetic variability in CMT results in variations in the clinical presentation and severity of the disease. Different gene mutations can affect different aspects of nerve function, leading to variability in symptoms and disease progression.
Genetic Subtype: The specific genetic subtype of CMT can influence the prognosis. Some subtypes may have a milder course with slower disease progression, while others may lead to more severe symptoms and faster disease progression.
Disease Severity at Diagnosis: The severity of symptoms and functional impairment can provide insights into the prognosis. Individuals with more severe initial symptoms may have a higher risk of disability and faster disease progression.
Electrophysiological Findings: Electrophysiological studies, such as nerve conduction studies and electromyography, can help assess the extent of nerve damage and demyelination. Severe electrophysiological abnormalities may indicate a worse prognosis.
Disease Progression Rate: The rate at which the disease progresses can vary among individuals with CMT. Faster disease progression may indicate a poorer prognosis.
Comorbidities: The presence of additional medical conditions or comorbidities can impact the overall prognosis and functional outcomes in individuals with CMT.
CLINICAL HISTORY
Age group:
CMT can present at any age, from early childhood to late adulthood.
The age of onset may vary depending on the specific subtype of CMT.
Some subtypes may have an early onset, while others may present later in life.
PHYSICAL EXAMINATION
Motor Examination:
Muscle weakness: Assess the strength of various muscle groups, especially in the lower limbs, such as hip flexors, knee extensors, ankle dorsiflexors, and toe extensors.
Muscle atrophy: Look for signs of muscle wasting, particularly in the lower legs and feet.
Foot deformities: Examine for high arches (pes cavus), hammer toes, or claw-like deformities.
Hand weakness: Assess grip strength and fine motor dexterity.
Sensory Examination:
Evaluate sensory function, including light touch, vibration sense, and proprioception, in the distal extremities.
Test for diminished or absent sensation, particularly in the feet and hands.
Reflexes:
Check deep tendon reflexes, such as the patellar reflex (knee jerk) and ankle reflex (Achilles reflex).
Look for signs of hyperreflexia or reduced reflexes.
Gait Assessment:
Observe the patient’s gait, noting any abnormalities such as foot drop, high stepping, or frequent tripping.
Assess balance and coordination during walking, turning, and other motor tasks.
Other Findings:
Evaluate the presence of associated features, such as scoliosis (spine curvature), pes planus (flat feet), or pes cavovarus (combination of high arches and inversion of the heel).
Associated Comorbidity or Activity:
Foot deformities: Many individuals with CMT develop foot deformities such as high arches (pes cavus) or flat feet.
Hand weakness: Weakness and muscle wasting in the hands may be present, affecting fine motor skills.
Sensory changes: Some individuals may experience sensory symptoms such as numbness, tingling, or decreased sensation in the extremities.
Balance and coordination issues: Problems with balance and coordination, leading to frequent tripping or difficulty walking on uneven surfaces.
Muscle weakness and atrophy: Weakness and wasting of the muscles, particularly in the lower legs, may be evident.
Acuity of Presentation:
CMT typically presents gradually and progresses slowly over time.
The rate of disease progression can vary among individuals, even within the same subtype of CMT.
Symptoms may start with mild weakness or sensory changes and progress to more pronounced muscle weakness and functional impairment.
DIFFERENTIAL DIAGNOSIS
Hereditary Neuropathies:
Hereditary motor and sensory neuropathy type I, II, III, IV, or X.
Distal hereditary motor neuropathies (DHUN)
Hereditary sensory and autonomic neuropathies (HSAN)
Physical therapy and rehabilitation to improve strength, balance, and mobility
Assistive devices such as orthopedic footwear, ankle-foot orthoses (AFOs), braces, or canes to aid in walking and prevent falls.
Occupational therapy to assist daily activities and adaptive strategies.
Administration of Pharmaceutical Agents:
Pain management with nonsteroidal anti-inflammatory drugs (NSAIDs) or other analgesics for neuropathic pain.
Medications to manage associated symptoms such as muscle cramps, muscle spasticity, or bladder dysfunction.
Interventional Procedures:
Surgical correction of foot deformities (e.g., pes cavus) to improve gait and prevent foot ulcers.
Nerve decompression surgery to relieve pressure on compressed nerves.
Tendon transfers or lengthening procedures to correct muscle imbalances and improve function.
Phase of Management:
Regular monitoring of disease progression and functional status.
Adjustment of treatment approaches as needed based on symptoms and functional limitations.
Ongoing collaboration with a multidisciplinary team including neurologists, physical therapists, occupational therapists, orthopedic surgeons, and genetic counsellors.
Charcot-Marie-Tooth Disease Madhu Nagappa; Shivani Sharma; Arun B Taly.ncbi.nlm.nih.gov
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