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Pathology - Nervous System Malformations
This guide summarizes common nervous system malformations, focusing on understanding their causes, presentations, and associated complications.
I. Neural Tube Defects (NTDs)
This guide summarizes common nervous system malformations, focusing on understanding their causes, presentations, and associated complications.
I. Neural Tube Defects (NTDs)
- Definition: Failure of the neural tube to close properly during embryogenesis (weeks 3-4).
- Etiology: Multifactorial – both genetic predisposition and environmental factors contribute. Maternal folate deficiency during early gestation is a significant risk factor.
- Types:
- Anencephaly: Fatal malformation; absence of brain and cranial vault. Anterior neural tube defect.
- Encephalocele: Protrusion of malformed brain tissue through a skull defect (often occipital). Large encephaloceles are usually fatal.
- Spina Bifida: Group of malformations due to incomplete closure of the caudal neural tube. Lack of fusion of vertebral arches and skin. Severity varies:
- Meningocele: Outpouching of meninges only.
- Myelomeningocele: Outpouching of meninges and spinal cord. Can cause urinary incontinence, constipation, and motor/sensory impairment in legs.
- Definition: Failure of the glial bridge to form between cerebral hemispheres, preventing axon crossing. Can be complete or partial.
- Association: Frequently occurs with other malformations.
- Presentation: Variable degrees of psychomotor retardation.
- Definition: Narrowing of the cerebral aqueduct.
- Etiology: Developmental anomaly; can be inherited (autosomal recessive or X-linked).
- Presentation: Congenital hydrocephalus (build-up of cerebrospinal fluid in the brain).
- Definition: Downward displacement of cerebellar structures into the foramen magnum.
- Type II (Arnold-Chiari): Severe; small posterior fossa, downward displacement of cerebellar vermis and medulla. Usually associated with lumbar myelomeningocele.
- Type I: Milder; cerebellar tonsils extend into the spinal canal. May be asymptomatic.
- Definition: Absent or rudimentary cerebellar vermis; large cyst (dilated fourth ventricle) fills the posterior fossa.
- Association: Often associated with other malformations.
- Definition: Fluid-filled cavity (syrinx) within the spinal cord's central grey matter.
- Location: Usually cervical and upper thoracic segments; extension into the medulla is called syringobulbia.
- Effect: Syrinx expansion causes adjacent spinal cord atrophy.
- Presentation: Typically presents in early adulthood with isolated loss of pain and temperature sensation in the upper limbs (due to spinothalamic tract damage).
- Embryological timing: Understand the developmental windows during which these malformations occur.
- Etiological factors: Recognize the interplay of genetic and environmental influences, particularly folate's role in NTDs.
- Clinical presentations: Learn to differentiate between the various malformations based on their symptoms and associated findings (e.g., hydrocephalus, motor deficits).
- Associated anomalies: Many of these malformations occur together, highlighting the interconnectedness of neural development.
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Pathology - Pemphigus vulgaris
Definition: An immunobullous dermatosis resulting from autoantibodies targeting epidermal desmosomal proteins.
Epidemiology • Infrequent, occurring at a rate of 0.1–1 per 100,000 individuals annually. • Typically impacts middle-aged persons aged 40–60 years.
Aetiology: Production of autoantibodies targeting the epidermal desmosomal cadherin, desmoglein-3.
Pathogenesis • The autoantibody attaches to the extracellular domain of desmoglein-3, resulting in desmosomal impairment and acantholysis. • The conventional perspective posited that complement fixation resulted in acantholysis; however, other researchers have proposed that acantholysis may arise via cytoskeletal collapse independent of complement activity.
Exposition • The majority of cases commence with oral erosions and blisters, then followed weeks or months later by the emergence of cutaneous lesions. The cutaneous lesions are delicate vesicles arising on unremarkable or erythematous skin. The blisters readily burst, resulting in a painful eroded region. • The skin lesions generally manifest on the face, scalp, axillae, and groin.
Histopathology • Biopsies reveal a blister cavity within the epidermis populated by acantholytic keratinocytes. • Generally, the cleavage occurs at a suprabasal level, resulting in the blister floor being lined by a solitary layer of intact basal keratinocytes. • Acantholysis may also affect the epidermis of adnexal structures. • Typically, there exists a fundamental dermal inflammatory infiltrate characterized by a significant presence of eosinophils.
Immunofluorescence
Direct immunofluorescence on perilesional skin demonstrates the deposition of IgG and C3 in the intercellular space of the epidermis.
Prognosis: Mortality rates are minimal with suitable immunosuppressive therapies. • The majority of problems are associated with therapy.
Definition: An immunobullous dermatosis resulting from autoantibodies targeting epidermal desmosomal proteins.
Epidemiology • Infrequent, occurring at a rate of 0.1–1 per 100,000 individuals annually. • Typically impacts middle-aged persons aged 40–60 years.
Aetiology: Production of autoantibodies targeting the epidermal desmosomal cadherin, desmoglein-3.
Pathogenesis • The autoantibody attaches to the extracellular domain of desmoglein-3, resulting in desmosomal impairment and acantholysis. • The conventional perspective posited that complement fixation resulted in acantholysis; however, other researchers have proposed that acantholysis may arise via cytoskeletal collapse independent of complement activity.
Exposition • The majority of cases commence with oral erosions and blisters, then followed weeks or months later by the emergence of cutaneous lesions. The cutaneous lesions are delicate vesicles arising on unremarkable or erythematous skin. The blisters readily burst, resulting in a painful eroded region. • The skin lesions generally manifest on the face, scalp, axillae, and groin.
Histopathology • Biopsies reveal a blister cavity within the epidermis populated by acantholytic keratinocytes. • Generally, the cleavage occurs at a suprabasal level, resulting in the blister floor being lined by a solitary layer of intact basal keratinocytes. • Acantholysis may also affect the epidermis of adnexal structures. • Typically, there exists a fundamental dermal inflammatory infiltrate characterized by a significant presence of eosinophils.
Immunofluorescence
Direct immunofluorescence on perilesional skin demonstrates the deposition of IgG and C3 in the intercellular space of the epidermis.
Prognosis: Mortality rates are minimal with suitable immunosuppressive therapies. • The majority of problems are associated with therapy.
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Pathology - Dermatitis herpetiformis
Definition: An immunobullous skin disorder marked by severe pruritus, papules, and vesicles, granular IgA deposition in the papillary dermis, and a significant correlation with celiac disease.
Epidemiology • Uncommon. The condition can afflict individuals of any age, while the highest frequency occurs in young people aged 20 to 40 years. Males are impacted twice as frequently as females. This illness is very prevalent in Northern Europe and Ireland. Up to 90% of individuals exhibit indications of celiac disease, although this may be asymptomatic.
Aetiology mediator. • IgA transglutaminase antibodies generated in the gastrointestinal tract seem to be pivotal.
Pathogenesis • IgA transglutaminase antibodies interact with transglutaminase enzymes present in the skin. The fixation of complement induces chemotaxis of neutrophils into the papillary dermis. • Enzymes secreted by neutrophils induce blister development.
Presentation • The rash consists of clusters of papules and vesicles that are highly pruritic. • Preferred locations are the shoulders, back, buttocks, elbows, and knees.
Histopathology Biopsies from first lesions reveal aggregates of neutrophils within the papillary dermis (papillary dermal microabscesses). Biopsies from established lesions reveal a subepidermal blister abundant in neutrophils. Immunofluorescence Direct immunofluorescence of perilesional skin demonstrates granular deposition of IgA in the papillary dermis.
Prognosis: The condition is typically chronic and persistent; nevertheless, it exhibits a significant response to the medication dapsone.
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Pathology - Bullous pemphigoid
It is an immunobullous dermatological condition characterized by the presence of autoantibodies targeting epidermal hemidesmosomal proteins.
Epidemiology • The most prevalent immunobullous skin disorder, however still an uncommon condition with an annual incidence of 7 per million individuals. • The majority of cases occur in older adults over the age of 70. Aetiology • Generation of autoantibodies targeting epidermal hemidesmosomal proteins. • The principal antigens are identified as BPAg1 and BPAg2.
Pathogenesis • Antibody binding results in complement fixation and the influx of inflammatory cells, notably eosinophils. • Direct cytotoxic effects disrupt the hemidesmosomes that anchor the epidermis to the dermis, causing complete separation of the epidermis from the dermis.
Presentation • Characteristic skin lesions consist of substantial, tight, intact blisters that arise on either normal or erythematous skin. • Preferred locations include the lower trunk, inner thighs, forearms, axillae, and groin regions.
Histopathology • Biopsies reveal a subepidermal blister populated by numerous eosinophils. • The underlying dermis exhibits edema and is infiltrated by a significant inflammatory response rich in eosinophils. Direct immunofluorescence on perilesional skin demonstrates linear deposition of IgG and C3 along the basement membrane zone.
Prognosis • Mortality rates remain low with suitable immunosuppressive protocols. • The majority of problems are associated with therapy.
It is an immunobullous dermatological condition characterized by the presence of autoantibodies targeting epidermal hemidesmosomal proteins.
Epidemiology • The most prevalent immunobullous skin disorder, however still an uncommon condition with an annual incidence of 7 per million individuals. • The majority of cases occur in older adults over the age of 70. Aetiology • Generation of autoantibodies targeting epidermal hemidesmosomal proteins. • The principal antigens are identified as BPAg1 and BPAg2.
Pathogenesis • Antibody binding results in complement fixation and the influx of inflammatory cells, notably eosinophils. • Direct cytotoxic effects disrupt the hemidesmosomes that anchor the epidermis to the dermis, causing complete separation of the epidermis from the dermis.
Presentation • Characteristic skin lesions consist of substantial, tight, intact blisters that arise on either normal or erythematous skin. • Preferred locations include the lower trunk, inner thighs, forearms, axillae, and groin regions.
Histopathology • Biopsies reveal a subepidermal blister populated by numerous eosinophils. • The underlying dermis exhibits edema and is infiltrated by a significant inflammatory response rich in eosinophils. Direct immunofluorescence on perilesional skin demonstrates linear deposition of IgG and C3 along the basement membrane zone.
Prognosis • Mortality rates remain low with suitable immunosuppressive protocols. • The majority of problems are associated with therapy.
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Pathology - Erythema multiforme
Definition: An inflammatory dermatosis characterized by unique targetoid lesions clinically and an interface reaction pattern histologically.
Epidemiology: • Fairly prevalent. • Primarily impacts the youth, encompassing youngsters.
Etiology • The majority of cases are associated with current or prior infections of the herpes simplex virus (HSV), which may not always be clinically evident. • Additional infectious organisms, such as Mycoplasma, have been implicated. • Pharmaceuticals are also acknowledged as a causative factor. Pathogenesis • Believed to signify a delayed-type hypersensitivity response to HSV antigens conveyed to the skin via circulating lymphocytes.
Presentation: Discrete circular erythematous patches, measuring 1–2 cm, with central darkening that may form blisters, referred to as 'target' lesions. • The majority of instances pertain to the extremities. • Mild oral involvement is prevalent.
Histopathology • Biopsies reveal interface dermatitis typified by a superficial lymphohistiocytic inflammatory infiltrate, substantial basal cell vacuolar degeneration, and keratinocyte death. • Instances of significant basal cell destruction may lead to subepidermal clefting and blister formation.
Prognosis: Most instances are self-limiting; however, recurring episodes are prevalent.
Definition: An inflammatory dermatosis characterized by unique targetoid lesions clinically and an interface reaction pattern histologically.
Epidemiology: • Fairly prevalent. • Primarily impacts the youth, encompassing youngsters.
Etiology • The majority of cases are associated with current or prior infections of the herpes simplex virus (HSV), which may not always be clinically evident. • Additional infectious organisms, such as Mycoplasma, have been implicated. • Pharmaceuticals are also acknowledged as a causative factor. Pathogenesis • Believed to signify a delayed-type hypersensitivity response to HSV antigens conveyed to the skin via circulating lymphocytes.
Presentation: Discrete circular erythematous patches, measuring 1–2 cm, with central darkening that may form blisters, referred to as 'target' lesions. • The majority of instances pertain to the extremities. • Mild oral involvement is prevalent.
Histopathology • Biopsies reveal interface dermatitis typified by a superficial lymphohistiocytic inflammatory infiltrate, substantial basal cell vacuolar degeneration, and keratinocyte death. • Instances of significant basal cell destruction may lead to subepidermal clefting and blister formation.
Prognosis: Most instances are self-limiting; however, recurring episodes are prevalent.
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Pathology - Granuloma annulare
Definition: An inflammatory dermatosis often characterized by annular lesions clinically and necrobiotic granulomatous inflammation histologically.
Epidemiology: Prevalent. Aetiology • Predominantly unknown in most instances. • Borrelia infection has been associated with a limited number of instances.
Pathogenesis • Current information indicates it constitutes a cutaneous reaction pattern to undefined antigens.
Presentation • Localized lesions of granuloma annulare manifest as flesh-colored or red papules that coalesce to form an annular lesion of 1–5 cm. • Acral regions are typically involved, particularly the knuckles and fingers.
Histopathology • The dermis exhibits a palisading granuloma, defined by a core region of degraded (necrobiotic) collagen encircled by radially oriented histiocytes, lymphocytes, and fibroblasts. • Mucin is frequently observed within the necrobiotic focal area. • Sometimes, the process results in a more nuanced ill-defined lesion in the dermis instead of a conventional well-formed palisaded granuloma (interstitial granuloma annulare).
Prognosis: Approximately 50% of cases resolve after two years of commencement, however recurrences are rather frequent.
Definition: An inflammatory dermatosis often characterized by annular lesions clinically and necrobiotic granulomatous inflammation histologically.
Epidemiology: Prevalent. Aetiology • Predominantly unknown in most instances. • Borrelia infection has been associated with a limited number of instances.
Pathogenesis • Current information indicates it constitutes a cutaneous reaction pattern to undefined antigens.
Presentation • Localized lesions of granuloma annulare manifest as flesh-colored or red papules that coalesce to form an annular lesion of 1–5 cm. • Acral regions are typically involved, particularly the knuckles and fingers.
Histopathology • The dermis exhibits a palisading granuloma, defined by a core region of degraded (necrobiotic) collagen encircled by radially oriented histiocytes, lymphocytes, and fibroblasts. • Mucin is frequently observed within the necrobiotic focal area. • Sometimes, the process results in a more nuanced ill-defined lesion in the dermis instead of a conventional well-formed palisaded granuloma (interstitial granuloma annulare).
Prognosis: Approximately 50% of cases resolve after two years of commencement, however recurrences are rather frequent.
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Pathology - Squamous cell carcinoma
Definition: A malignant epidermal tumor with squamous differentiation.
Epidemiology: Common tumors constitute around 15% of all skin cancers. • The majority occur on sun-exposed skin of older individuals with fair complexions.
Aetiology • The majority are associated with cumulative exposure to UV radiation. • Immunosuppression elevates the risk. Transplant recipients are especially susceptible to the development of numerous tumors. Carcinogenesis • The majority originate from actinic keratoses, which are dysplastic epidermal lesions that develop on sun-damaged skin. UV light, especially UVB, causes DNA damage in genes that regulate development, such as KRAS and CDK4.
Presentation • Dermal plaques or nodules, frequently exhibiting a keratinized surface crust. • Ulceration may occur.
Histopathology • Atypical squamous epithelial cells are observed in nests, sheets, and cords, originating from the epidermis and infiltrating the underlying dermis. • Tumors are classified as well, moderately, or poorly differentiated based on the degree of keratinization.
Prognosis: • The majority are primarily locally infiltrative upon diagnosis and can be effectively treated with surgical excision. Factors contributing to recurrence or metastasis encompass invasion depth, poor differentiation, perineural invasion, restricted excision, and immunosuppression.
Pathological classification of cutaneous carcinomas Primary tumor (T) pT1: tumor is 2 cm or smaller in diameter. pT2: tumor exceeds 2 cm in size. pT3: tumor infiltrates muscle, bone, cartilage, jaws, and orbit. pT4: tumor infiltrates the skull base and axial skeleton. Regional lymphatic nodes (N) pN1: solitary nodal metastasis measuring less than 3 cm in size. pN2: solitary nodal metastasis ranging from 3 to 6 cm in size or several nodal metastases, with none exceeding 6 cm. pN3: any nodal metastasis over 6 cm
Definition: A malignant epidermal tumor with squamous differentiation.
Epidemiology: Common tumors constitute around 15% of all skin cancers. • The majority occur on sun-exposed skin of older individuals with fair complexions.
Aetiology • The majority are associated with cumulative exposure to UV radiation. • Immunosuppression elevates the risk. Transplant recipients are especially susceptible to the development of numerous tumors. Carcinogenesis • The majority originate from actinic keratoses, which are dysplastic epidermal lesions that develop on sun-damaged skin. UV light, especially UVB, causes DNA damage in genes that regulate development, such as KRAS and CDK4.
Presentation • Dermal plaques or nodules, frequently exhibiting a keratinized surface crust. • Ulceration may occur.
Histopathology • Atypical squamous epithelial cells are observed in nests, sheets, and cords, originating from the epidermis and infiltrating the underlying dermis. • Tumors are classified as well, moderately, or poorly differentiated based on the degree of keratinization.
Prognosis: • The majority are primarily locally infiltrative upon diagnosis and can be effectively treated with surgical excision. Factors contributing to recurrence or metastasis encompass invasion depth, poor differentiation, perineural invasion, restricted excision, and immunosuppression.
Pathological classification of cutaneous carcinomas Primary tumor (T) pT1: tumor is 2 cm or smaller in diameter. pT2: tumor exceeds 2 cm in size. pT3: tumor infiltrates muscle, bone, cartilage, jaws, and orbit. pT4: tumor infiltrates the skull base and axial skeleton. Regional lymphatic nodes (N) pN1: solitary nodal metastasis measuring less than 3 cm in size. pN2: solitary nodal metastasis ranging from 3 to 6 cm in size or several nodal metastases, with none exceeding 6 cm. pN3: any nodal metastasis over 6 cm
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Pathology - Malignant melanoma
A malignant melanocytic tumor.
Epidemiology • Less prevalent than basal or squamous cell carcinomas of the skin, however far more lethal. • Primarily observed in those with pale skin who have been exposed to sunlight.
Aetiology • Intermittent exposure to high doses of UV radiation constitutes the primary risk factor. • A component of genetic predisposition may also be pertinent. Genetics • Melanomas that develop in areas intermittently exposed to sunlight generally exhibit mutations in BRAF as an initial genetic occurrence. • Progression correlates with the accumulation of mutations in genes such as KIT, MITF, CDKN2A, TP53, and PTEN. • The majority also have chromosomal abnormalities characterized by gains and/or losses of chromosomal segments.
Presentation • The majority of melanomas manifest as pigmented cutaneous lesions exhibiting A symmetry, irregular B ordering, heterogeneous C olour, and D iameter exceeding 6mm (the ‘ABCD’ abbreviation).
Histopathology • A characteristic feature of all types of malignant melanoma is the existence of a neoplastic proliferation of markedly abnormal melanocytes. If the process is restricted to the epidermis, the term melanoma in situ may be utilized. • The term invasive melanoma may be utilized once penetration into the dermis has transpired.
Evolution • The majority of melanomas initially develop as a flat lesion in a radial manner, referred to as the radial growth phase. In this phase, there is either an absence of dermal invasion or the cells within the dermis are incapable of surviving and proliferating. • As advancement occurs, the growth transitions, enabling cells inside the dermis to proliferate. This phase is referred to as the vertical growth phase and is linked to the development of metastatic potential
Prognosis: Survival correlates with the disease stage at the time of diagnosis. • The primary factors determining the stage are the Breslow thickness of the melanoma and the presence of ulceration. • The mitotic rate is also acknowledged as a significant prognostic predictor in vertical growth phase melanomas.
A malignant melanocytic tumor.
Epidemiology • Less prevalent than basal or squamous cell carcinomas of the skin, however far more lethal. • Primarily observed in those with pale skin who have been exposed to sunlight.
Aetiology • Intermittent exposure to high doses of UV radiation constitutes the primary risk factor. • A component of genetic predisposition may also be pertinent. Genetics • Melanomas that develop in areas intermittently exposed to sunlight generally exhibit mutations in BRAF as an initial genetic occurrence. • Progression correlates with the accumulation of mutations in genes such as KIT, MITF, CDKN2A, TP53, and PTEN. • The majority also have chromosomal abnormalities characterized by gains and/or losses of chromosomal segments.
Presentation • The majority of melanomas manifest as pigmented cutaneous lesions exhibiting A symmetry, irregular B ordering, heterogeneous C olour, and D iameter exceeding 6mm (the ‘ABCD’ abbreviation).
Histopathology • A characteristic feature of all types of malignant melanoma is the existence of a neoplastic proliferation of markedly abnormal melanocytes. If the process is restricted to the epidermis, the term melanoma in situ may be utilized. • The term invasive melanoma may be utilized once penetration into the dermis has transpired.
Evolution • The majority of melanomas initially develop as a flat lesion in a radial manner, referred to as the radial growth phase. In this phase, there is either an absence of dermal invasion or the cells within the dermis are incapable of surviving and proliferating. • As advancement occurs, the growth transitions, enabling cells inside the dermis to proliferate. This phase is referred to as the vertical growth phase and is linked to the development of metastatic potential
Prognosis: Survival correlates with the disease stage at the time of diagnosis. • The primary factors determining the stage are the Breslow thickness of the melanoma and the presence of ulceration. • The mitotic rate is also acknowledged as a significant prognostic predictor in vertical growth phase melanomas.
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Pathology - Mycosis fungoides
A low-grade T-cell lymphoma characterized by variably epidermotropic skin-homing T-lymphocytes.
Epidemiology: The most prevalent type of primary cutaneous lymphoma, however it remains a rare condition, impacting 0.3 individuals per 100,000 yearly. • Typically an affliction of maturity, however it may sporadically impact children.
Aetiology: Unknown. Genetics • The course of the disease correlates with chromosomal abnormalities, especially those involving chromosomes 8 and 17.
Presentation • Defined by the progressive emergence of patches, plaques, and tumors on non-sun-exposed skin, mainly in the regions of the buttocks and trunk.
Patches are several extensive (> 10mm) flat erythematous scaly sores.
• Plaques are raised lesions that may arise inside existing patches or develop independently.
• Tumour nodules and, at times, erythroderma may subsequently arise. • Advanced illness may affect the bone marrow, lymph nodes, and visceral organs.
Histopathology The patch stage has a modest upper dermal T-cell infiltrate accompanied by variable epidermotropism. The early stages of the disease are frequently challenging to detect due to overlapping characteristics with many inflammatory disorders. • The plaque stage has a more pronounced, band-like infiltration of T-cells with increased epidermotropism. Aggregates of neoplastic cells within the epidermis are commonly observed (Pautrier microabscesses). The nuclear atypia of the lymphocytes is more pronounced. The tumor stage indicates a more widespread skin infiltrate that may migrate into the subcutaneous fat. Epidermotropism may be diminished. Immunophenotype: Most instances exhibit a T-helper cell phenotype, specifically CD3 + CD4 + CD8–.
Prognosis: The likelihood of progression and mortality is associated with the illness stage at presentation. • The 10-year survival rates are elevated (85–95%) in patch and plaque stage disease, decreasing to 40% in tumor stage, and to 20% with nodal involvement.
A low-grade T-cell lymphoma characterized by variably epidermotropic skin-homing T-lymphocytes.
Epidemiology: The most prevalent type of primary cutaneous lymphoma, however it remains a rare condition, impacting 0.3 individuals per 100,000 yearly. • Typically an affliction of maturity, however it may sporadically impact children.
Aetiology: Unknown. Genetics • The course of the disease correlates with chromosomal abnormalities, especially those involving chromosomes 8 and 17.
Presentation • Defined by the progressive emergence of patches, plaques, and tumors on non-sun-exposed skin, mainly in the regions of the buttocks and trunk.
Patches are several extensive (> 10mm) flat erythematous scaly sores.
• Plaques are raised lesions that may arise inside existing patches or develop independently.
• Tumour nodules and, at times, erythroderma may subsequently arise. • Advanced illness may affect the bone marrow, lymph nodes, and visceral organs.
Histopathology The patch stage has a modest upper dermal T-cell infiltrate accompanied by variable epidermotropism. The early stages of the disease are frequently challenging to detect due to overlapping characteristics with many inflammatory disorders. • The plaque stage has a more pronounced, band-like infiltration of T-cells with increased epidermotropism. Aggregates of neoplastic cells within the epidermis are commonly observed (Pautrier microabscesses). The nuclear atypia of the lymphocytes is more pronounced. The tumor stage indicates a more widespread skin infiltrate that may migrate into the subcutaneous fat. Epidermotropism may be diminished. Immunophenotype: Most instances exhibit a T-helper cell phenotype, specifically CD3 + CD4 + CD8–.
Prognosis: The likelihood of progression and mortality is associated with the illness stage at presentation. • The 10-year survival rates are elevated (85–95%) in patch and plaque stage disease, decreasing to 40% in tumor stage, and to 20% with nodal involvement.
