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Human Anatomy · General anatomy

Skin, and How the Body Forms

Skin is the organ you touch at every treatment and the one that records what went wrong. Development explains why a nerve root supplies both a strip of skin and a set of muscles, and why pain from a deep organ is felt somewhere else entirely.

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Part 1 · General anatomy

Skin layers and repair, the germ layers, and why one nerve root has both a muscle and a skin patch

Two subjects in one chapter, and why they belong together

Skin is the organ you touch every time you treat a patient, the organ that fails first in the immobile, and the organ whose repair you either help or hinder. Embryology is what explains why the body is organised the way it is — why a nerve root supplies both a strip of skin and a group of muscles, why cardiac pain is felt in the left arm, why the ureter and the testis share a pain pathway, and why the thumb is lateral and the great toe medial.

They belong in one chapter because the answer to the chapter’s subtitle question — why one nerve root has both a muscle and a skin patch — comes from development, and is the single most clinically useful idea in either subject.

Learning outcomes

  • Describe the layers of the epidermis and dermis and their cell populations.
  • Describe skin appendages and skin blood supply, and explain thermoregulation.
  • Describe the phases and timeline of wound healing, and distinguish healing by primary and secondary intention.
  • Explain scar maturation and the difference between hypertrophic and keloid scar.
  • Classify burns and pressure injuries and state the physiotherapy implications of each.
  • Describe the formation of the three germ layers and name the derivatives of each.
  • Describe somite formation and differentiation into sclerotome, myotome and dermatome.
  • Explain segmentation, and define dermatome, myotome, sclerotome and viscerotome.
  • Explain referred pain and the shoulder-tip / cardiac / diaphragmatic referral patterns from developmental principles.
  • Describe limb development, including the AER, ZPA and limb rotation.
  • Recognise the common congenital conditions a physiotherapist will meet.

Part A · Skin

The integument in numbers

Figure 1 · What skin does

What skin does Six panels naming the functions of skin: barrier, sensation, temperature regulation, vitamin D, immune defence and repair. THE LARGEST ORGAN YOU HAVE, AND IT DOES SIX JOBS Barrier Keeps water in and organisms out Sensation Touch, pressure, vibration, temperature, pain Temperature Sweating and blood flow regulate heat loss Vitamin D Made in the skin under ultraviolet light Immune defence Cells in the epidermis present invaders Repair Heals itself, and regrows from the edges and appendages
You assess it on every patient, whether you mean to or not. Colour, temperature, texture and integrity are all information before you have asked a question.

Skin is the largest organ: 1.5–2 m² in an adult, ~15% of body weight, thickness from 0.5 mm on the eyelid to 4–5 mm on the sole and palm.

Its functions: protection (mechanical, chemical, microbial, ultraviolet), thermoregulation, sensation, vitamin D synthesis, fluid and electrolyte conservation, immune surveillance, excretion, absorption (the basis of transdermal drug delivery and of many topical physiotherapy agents), and social and communicative function.

Skin is classified as thick (palms and soles: thick epidermis with a stratum lucidum, no hair follicles or sebaceous glands, abundant sweat glands, epidermal ridges producing fingerprints) or thin (everywhere else: thinner epidermis, hair follicles and sebaceous glands present).

Structure

Figure 2 · The structure of the skin

A block of skin cut away to show the epidermis, dermis and hypodermis, with the layers of the epidermis named in order, the hair follicle with its sebaceous gland and arrector pili muscle, the sweat glands, and the sensory endings drawn separately with what each one detects.
Three layers, and everything else sits within them. The sensory endings are the part that matters most to a physiotherapist, because they are what you are stimulating whenever you touch a patient.

8.3.1 Epidermis — stratified squamous keratinised epithelium, ectodermal, avascular

From deep to superficial:

LayerFeatures
Stratum basale (germinativum)A single layer of columnar cells on the basement membrane; the mitotic layer. Contains melanocytes, Merkel cells and epidermal stem cells
Stratum spinosumSeveral layers of polyhedral keratinocytes joined by desmosomes (the “prickles”); contains Langerhans cells
Stratum granulosum3–5 layers with keratohyalin granules (filaggrin) and lamellar bodies releasing lipid — the water barrier is formed here
Stratum lucidumA clear layer, present only in thick skin
Stratum corneum15–30 layers of anucleate, flattened, keratin-filled corneocytes in a lipid matrix; continuously desquamated

Epidermal turnover is approximately 28–40 days from basal cell to desquamation — accelerated dramatically in psoriasis (to ~4–7 days), which is why psoriatic plaques are scaly.

Non-keratinocyte cells:

CellOriginFunction
MelanocyteNeural crestProduces melanin in melanosomes, transferred to keratinocytes to shield nuclear DNA from UV. Skin colour reflects melanin type and distribution, not melanocyte number, which is similar across populations
Langerhans cellBone marrowDendritic antigen-presenting cell; the afferent limb of contact hypersensitivity
Merkel cellNeural crest / epidermalSlowly adapting type I mechanoreceptor; light touch and texture discrimination

8.3.2 Dermis — mesodermal, vascular

LayerStructure
Papillary dermisLoose connective tissue forming dermal papillae that interdigitate with epidermal ridges (increasing adhesion and surface area for diffusion); contains capillary loops and Meissner’s corpuscles
Reticular dermisDense irregular connective tissue: thick type I collagen bundles and elastic fibres; contains appendages, Pacinian and Ruffini corpuscles, vessels and nerves

The predominant collagen bundle orientation in the reticular dermis creates lines of cleavage (Langer’s lines). Incisions parallel to them gape less and scar better; incisions across them gape and produce wider scars. Wound orientation relative to these lines partly predicts scar quality — a point of direct relevance in scar management.

Ageing skin shows epidermal thinning, flattening of the dermo-epidermal junction (reducing adhesion and increasing shear vulnerability — the reason elderly skin tears with adhesive tape removal), collagen and elastin loss, reduced vascularity, reduced sweat and sebaceous output, and slower healing.

8.3.3 Appendages

AppendageNotes
Hair follicleEpidermal downgrowth; cycles through anagen (growth), catagen, telogen (rest). Arrector pili is smooth muscle, sympathetically innervated
Sebaceous glandHolocrine; opens into the follicle; sebum lubricates and is antimicrobial; androgen-sensitive (hence acne)
Eccrine sweat glandMerocrine; over the whole body, densest on palms, soles and forehead; sympathetic cholinergic innervation (the exception to the adrenergic rule); the principal thermoregulatory effector; 2–4 million glands producing up to several litres per hour in extreme conditions
Apocrine sweat glandAxilla, areola, perineum; opens into hair follicles; active from puberty; odour results from bacterial action on the secretion
NailKeratinised plate; grows ~3 mm/month (fingernails) from the matrix under the lunula

8.3.4 Blood supply and thermoregulation

Two horizontal plexuses — deep (at the dermo-hypodermal junction) and superficial (subpapillary) — connected by perforating vessels, with arteriovenous anastomoses (glomus bodies) in the digits, palms, soles, ears and nose.

Skin blood flow can vary from about 0.5% to 30% of cardiac output. Sympathetic vasoconstrictor tone controls it; heat causes vasodilatation and sweating, cold causes vasoconstriction and arteriovenous shunting to preserve core temperature.

Clinical implications for physiotherapy: all thermal and electrophysical agents act on and through this system. In any patient with impaired sensation, impaired circulation or impaired cognition, the protective withdrawal from a damaging thermal stimulus is absent — which is why thermal agents are contraindicated over areas of sensory loss, arterial insufficiency, or in a patient who cannot report sensation reliably. Burns from hot packs and paraffin in neuropathic feet remain a persistent and entirely avoidable source of harm.

8.3.5 Cutaneous sensation

ReceptorAdaptationModality
Merkel discSlowly adapting type ISustained light touch, edges, texture; small receptive field
Meissner corpuscleRapidly adapting type ILight touch, low-frequency flutter, slip detection; dense in fingertips
Pacinian corpuscleRapidly adapting type IIHigh-frequency vibration, deep pressure; large receptive field
Ruffini endingSlowly adapting type IISkin stretch, sustained pressure, joint position contribution
Free nerve endingsNon-adaptingNociception (Aδ and C), temperature, crude touch, itch
Hair follicle receptorsRapidly adaptingHair movement

Two-point discrimination — approximately 2–4 mm on the fingertip, 40–50 mm on the back — reflects receptor density and cortical representation, and is a standard clinical measure of peripheral nerve regeneration.

Wound healing

The phases

PhaseTimingEventsPhysiotherapy implication
HaemostasisMinutesVasoconstriction, platelet plug, fibrin clot; platelets release PDGF, TGF-β
Inflammation~0–5 days (up to 7)Vasodilatation, increased permissibility; neutrophils (24–48 h) then macrophages (48–72 h, the key orchestrating cell); debridementProtect; manage oedema; maintain adjacent joint range
Proliferation~3 days – 3 weeksFibroplasia (type III collagen), angiogenesis, granulation tissue, epithelialisation (from wound edges and appendage remnants), wound contraction by myofibroblastsBegin controlled movement; protect the fragile new epithelium from shear
Remodelling (maturation)3 weeks – 1–2 yearsType III replaced by type I; fibres realign along stress lines; cross-links mature; vascularity and cellularity decline; the scar pales and softensThe phase physiotherapy influences most: scar mobilisation, sustained low-load stretch, pressure therapy, silicone, and progressive functional loading

Tensile strength timeline (a frequently examined sequence): ~5% at 1 week, ~20% at 3 weeks, ~50–60% at 6 weeks, and a plateau at ~70–80% of the original at 6–12 months. Scar never regains normal strength, and it lacks appendages, elastic recovery and normal sensation.

Primary versus secondary intention: a clean approximated wound heals by primary intention — minimal granulation, minimal contraction, a fine scar. A wound with tissue loss or contamination heals by secondary intention — abundant granulation, marked wound contraction, prolonged epithelialisation and a broad scar. Secondary healing is where contracture, and therefore physiotherapy, matters most.

Factors impairing healing: age; malnutrition (protein, vitamin C, zinc); diabetes; smoking; corticosteroids and immunosuppression; ischaemia and venous insufficiency; infection; repeated mechanical shear and pressure; radiotherapy; and foreign material.

Abnormal scar

Hypertrophic scarKeloid
ExtentRemains within the original wound boundaryExtends beyond the original wound
OnsetWithin weeksMay be months later
CourseOften improves over 1–2 yearsRarely regresses; recurs after excision
SitesAcross flexor surfaces, joints, high-tension areasSternum, shoulder, ear lobe, jaw
PredispositionAny; burns, prolonged healingGenetic; more common in darker-skinned individuals
ManagementPressure garments, silicone, massage, stretch, sustained positioning, splintingThe same plus intralesional corticosteroid; excision alone is not advised

Scar management principles for physiotherapy: sustained low-load stretch and positioning (exploiting creep — Chapter 7), pressure therapy (24 mmHg or more, worn 23 hours a day for months in burns), silicone gel or sheeting, massage once epithelialisation is complete, splinting in the anti-deformity position, and desensitisation. All of this works during the remodelling phase, which is the window that closes.

Burns

Depth classification

DepthLayers involvedAppearanceSensationHealing
Superficial (1st degree)Epidermis onlyErythema, dry, no blistersPainful3–7 days, no scar
Superficial partial (2nd, superficial dermal)Epidermis + papillary dermisBlisters, moist, pink, blanchesVery painful1–3 weeks, minimal scar
Deep partial (2nd, deep dermal)Into reticular dermisBlotchy red/white, less blanching, drierReduced sensation3–8 weeks; hypertrophic scarring likely; often grafted
Full thickness (3rd)Entire dermis ± appendagesWhite, waxy, leathery, charred; does not blanchInsensateWill not heal without grafting; contracture guaranteed
Fourth degreeInto fascia, muscle, boneCharred, exposed deep structuresInsensateSurgical; often amputation

Extent is estimated by the rule of nines in adults (head 9%, each arm 9%, each leg 18%, anterior trunk 18%, posterior trunk 18%, perineum 1%) — modified in children, whose head is proportionally larger; the Lund and Browder chart is more accurate.

Physiotherapy in burns is dominated by two aims: preventing contracture (positioning in the anti-deformity position — neck extension, shoulder abduction to ~90° with slight horizontal flexion, elbow extension and forearm supination, wrist slight extension with MCPs flexed to 70–90° and IPs extended, hips extended and abducted, knees extended, ankles neutral — which is the opposite of the comfortable flexed posture the patient adopts), and maintaining respiratory and functional capacity. Splinting, sustained stretch, early mobilisation, and later pressure therapy and scar management are the core interventions, delivered over months.

Pressure injury

Mechanism. Sustained pressure exceeding capillary closing pressure (~32 mmHg) occludes perfusion; shear compounds it by distorting and occluding vessels obliquely; moisture macerates and reduces tissue tolerance; friction removes the stratum corneum. Muscle is more susceptible than skin, so damage is frequently deeper than it appears — the “iceberg” pattern.

Sites: sacrum, ischial tuberosities, greater trochanters, heels, lateral malleoli, occiput, scapulae, elbows; and, increasingly, device-related sites (oxygen tubing, catheters, casts).

Staging (NPIAP/EPUAP):

StageDescription
1Intact skin with non-blanchable erythema
2Partial-thickness loss with exposed dermis; a shallow open ulcer or intact/ruptured blister
3Full-thickness skin loss; subcutaneous fat visible; no exposed bone, tendon or muscle
4Full-thickness skin and tissue loss; exposed bone, tendon or muscle
UnstageableBase obscured by slough or eschar
Deep tissue injuryPersistent non-blanchable deep red, maroon or purple discoloration, or a blood-filled blister

Prevention is the physiotherapy contribution, and it is substantial: repositioning schedules, pressure-redistributing surfaces, teaching independent pressure relief (lift-offs or leans every 15–30 minutes in wheelchair users), wheelchair seating and cushion prescription, transfer technique that eliminates dragging, maintaining mobility and nutrition, and skin inspection education. A stage 4 pressure injury in a spinal cord injured patient can cost a year of rehabilitation progress.

Part B · How the Body Forms

The first three weeks

Figure 3 · Neurulation and the neural crest

Four cross-sections of the embryo showing the neural tube forming Labelled: Neural plate, Surface ectoderm, Notochord, Mesoderm, Endoderm, Neural groove, Neural fold, Neural crest, Neural tube, Crest cells migrating. Neural plateSurface ectodermNotochordMesodermEndodermNeural grooveNeural foldNeural crestNeural tubeCrest cells migrating
The tube sinks beneath the surface and the crest cells leave it. Those migrating cells become sensory and autonomic ganglia, Schwann cells, the adrenal medulla and much of the face — which is why one population explains so many unrelated-looking structures. Illustration produced to brief; every label placed and checked by the Physiotherapist India Team.
StageTimingEvent
FertilisationDay 0Zygote formed in the ampulla of the uterine tube
Cleavage → morulaDays 1–4Successive divisions
BlastocystDays 5–6Inner cell mass (embryoblast) + trophoblast + blastocyst cavity
ImplantationDays 6–10In the uterine endometrium
Bilaminar discWeek 2Epiblast and hypoblast; amniotic cavity and yolk sac form. “The week of twos”
GastrulationWeek 3The primitive streak appears; epiblast cells migrate through it to form the three germ layers. “The week of threes”
NeurulationWeeks 3–4Notochord induces the overlying ectoderm to form the neural plate → neural groove → neural tube; neural crest cells separate

Gastrulation is the pivotal event: it converts a two-layered disc into a three-layered embryo with an established body plan and axes. Every tissue in the body traces to one of the three layers formed in that week.

The three germ layers and their derivatives

Figure 4 · The three germ layers and what each becomes

The three germ layers and what each becomes Ectoderm, mesoderm and endoderm listed with their adult derivatives. EVERY TISSUE IN THE BODY COMES FROM ONE OF THREE LAYERS ECTODERM the outside, and the nervous system Epidermis, hair, nails, sweat and sebaceous glands Whole nervous system: brain, cord, peripheral nerves Neural crest: sensory ganglia, autonomic ganglia, Schwann cells, adrenal medulla, melanocytes, much of the face Lens, inner ear, tooth enamel MESODERM everything in between, and most of what you treat Bone, cartilage, all connective tissue All muscle: skeletal, cardiac, smooth Heart, blood vessels, blood cells Kidneys, gonads, dermis ENDODERM the linings of the tubes Lining of the gut from pharynx to rectum Lining of the airways and lungs Liver, pancreas, thyroid, thymus Lining of the bladder and urethra
Mesoderm is the physiotherapist's layer. Bone, cartilage, connective tissue and every kind of muscle come from it.
Germ layerDerivatives
Ectoderm — surfaceEpidermis, hair, nails, sweat and sebaceous glands, mammary glands; lens and cornea epithelium; enamel of teeth; anterior pituitary; inner ear epithelium; epithelium of the mouth and anal canal below the pectinate line
Ectoderm — neuroectoderm (neural tube)Brain, spinal cord, retina and optic nerve, posterior pituitary, pineal gland, motor neurons, preganglionic autonomic neurons
Ectoderm — neural crestAn extraordinary list: dorsal root and autonomic ganglia, Schwann cells, adrenal medulla, melanocytes, enteric nervous system, meninges (pia and arachnoid), most of the skull and facial skeleton (via ectomesenchyme), odontoblasts, aorticopulmonary septum, parafollicular C cells
Mesoderm — paraxial (somites)Sclerotome → vertebrae, ribs, part of the skull base; Myotome → skeletal muscle; Dermatome → dermis and hypodermis of the back
Mesoderm — intermediateKidneys, ureters, gonads, genital ducts
Mesoderm — lateral plate (somatic)Limb bones, connective tissue and dermis of the limbs and body wall; parietal serous membranes
Mesoderm — lateral plate (splanchnic)Heart, blood and lymphatic vessels, blood cells, spleen, smooth muscle and connective tissue of the gut, visceral serous membranes, suprarenal cortex
EndodermEpithelial lining of the gastrointestinal and respiratory tracts; liver, pancreas, gallbladder; thyroid, parathyroid, thymus; bladder and urethral epithelium; tympanic cavity and auditory tube; tonsils

Neural crest — the “fourth germ layer”

Neural crest cells delaminate from the crests of the neural folds and migrate widely. Because they produce structures as unrelated as the facial skeleton, the adrenal medulla and skin melanocytes, a neurocristopathy produces baffling multi-system combinations: Hirschsprung disease (absent enteric ganglia), neurofibromatosis, Waardenburg syndrome (pigmentary changes with deafness), DiGeorge syndrome (thymic, parathyroid and conotruncal cardiac defects), and CHARGE syndrome. If you ever wonder why a child with a cardiac outflow defect also has a facial anomaly and pigmentary change, the answer is neural crest.

Somites and segmentation — the key to clinical anatomy

Figure 5 · What a somite becomes

What a somite becomes A somite dividing into sclerotome, myotome and dermatome, explaining the segmental pattern of nerve supply. SOMITE one block of mesoderm Sclerotome Vertebrae and ribs The bone around the cord Myotome Skeletal muscle of that segment The muscles a nerve root supplies Dermatome Dermis of the skin over it The skin patch a nerve root supplies One somite supplies one segment. That is why a single nerve root has a muscle group AND a skin patch, and why a root problem shows up in both at once.
This is why dermatomes and myotomes exist. One somite makes the bone, muscle and skin of one segment, and one nerve root grows out to serve it.

From day 20, paraxial mesoderm on each side of the notochord segments into somites, forming craniocaudally at roughly three pairs per day, reaching 42–44 pairs (4 occipital, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 8–10 coccygeal, several of which regress). Somite count is the standard measure of embryonic age in weeks 4–5.

Each somite differentiates into three parts:

PartBecomes
Sclerotome (ventromedial)Vertebrae, ribs, and their ligaments; migrates around the notochord and neural tube
Myotome (dorsolateral)Skeletal muscle — dividing into a dorsal epimere (innervated by the dorsal ramus, becoming the deep back extensors) and a ventral hypomere (innervated by the ventral ramus, becoming everything else)
Dermatome (dorsolateral, superficial)Dermis of the back; limb and ventral body wall dermis derives from lateral plate mesoderm, though it retains segmental innervation

Each somite is supplied by its own spinal nerve, and that relationship is retained for life however far the tissue migrates. This is the whole basis of segmental clinical anatomy.

The four “-tomes”

TermDefinitionClinical use
DermatomeThe area of skin supplied by a single spinal nerve rootSensory level in spinal cord injury; radiculopathy mapping; shingles distribution
MyotomeThe muscle group supplied by a single spinal nerve rootMotor level testing; root versus peripheral nerve localisation
SclerotomeThe bone and deep tissue derived from one somite and supplied by that rootExplains deep, poorly localised, aching bone pain that does not follow a dermatome
ViscerotomeThe viscera whose afferents enter at a given spinal levelThe basis of referred visceral pain

Dermatome maps do not agree with each other (Keegan and Garrett vs Foerster vs the modern evidence-based maps), because there is substantial overlap between adjacent dermatomes — usually enough that section of a single dorsal root produces little detectable sensory loss, and at least two adjacent roots must be lost for a definite area of anaesthesia. Use dermatomes as a probabilistic guide, not a map with fixed borders. The most reliable single points (C5 lateral elbow, C6 thumb, C7 middle finger, C8 little finger, T4 nipple, T10 umbilicus, L1 groin, L3 medial knee, L4 medial malleolus, L5 dorsum of foot / first web space, S1 lateral heel) are the ones worth memorising, and are the ASIA key sensory points.

Referred pain, explained developmentally

Visceral afferents accompany sympathetic fibres back to the spinal cord and converge on the same second-order neurons as somatic afferents from the corresponding dermatome. The brain, which receives far more somatic than visceral input over a lifetime, misattributes the signal to the skin — the convergence–projection theory.

StructureReferred toSegmentsDevelopmental explanation
HeartCentral chest, left arm and medial forearm, jawT1–T5Cardiac afferents enter at the same levels as the medial arm dermatomes
Diaphragm (central part)Tip of the shoulderC3, C4, C5 via the phrenic nerveThe diaphragm develops in the cervical region from the septum transversum at C3–C5 and migrates caudally, dragging its nerve supply. This is why splenic rupture, subphrenic abscess, hepatic irritation or gas after laparoscopy all present as shoulder-tip pain
Diaphragm (peripheral part)Lower chest wall and upper abdomenT7–T11 (intercostal nerves)Peripheral diaphragm acquires segmental innervation locally
GallbladderRight hypochondrium, inferior angle of the right scapulaT7–T9
UreterLoin to groin, testis or labiumT11–L2The gonad develops on the posterior abdominal wall at T10 and descends, retaining its nerve supply
Testis / ovaryPeriumbilical / loinT10Same reason — descent from the T10 level
AppendixPeriumbilical initially, then right iliac fossaT10 visceral → then somatic parietal peritoneumThe shift from vague central to localised right-sided pain is the classic diagnostic sequence
Hip jointKneeL2–L4 via the obturator nerveHilton’s law and shared segmental supply

Why this matters in a physiotherapy clinic

You will see patients presenting with musculoskeletal-sounding pain of visceral origin. Left shoulder or interscapular pain that is exertional, unrelated to position or movement, and accompanied by breathlessness or nausea is a cardiac presentation until proved otherwise. Right shoulder-tip pain with abdominal tenderness may be hepatobiliary or a ruptured viscus. Thoracic pain with a band-like distribution and no mechanical behaviour may be visceral or neoplastic.

The screening rule: musculoskeletal pain has a mechanical behaviour — it is reproduced and eased by specific positions and movements. Pain that is entirely unrelated to position, load or movement, or that is accompanied by systemic features, requires medical screening before it receives a mechanical diagnosis.

Limb development

Figure 6 · Limb development and rotation

The limb buds before rotation, the direction each one turns, and the finished arrangement, showing the upper limb rotating laterally and the lower limb medially through about ninety degrees, with the consequences for elbow, knee, extensor muscles, thumb and great toe.
The limbs rotate in opposite directions, and that single fact explains the adult layout. The upper limb turns outwards, carrying the elbow backwards and the thumb to the lateral side; the lower turns inwards, carrying the knee forwards and the great toe to the medial side.
StageTimingEvent
Limb bud appearsWeek 4 (upper) and shortly after (lower)Proliferation of lateral plate somatic mesoderm covered by ectoderm; myogenic cells migrate in from adjacent somites
Apical ectodermal ridge (AER)Weeks 4–8A thickened ectodermal ridge at the bud apex; controls proximodistal outgrowth via FGFs. Removal truncates the limb
Zone of polarising activity (ZPA)Posterior mesenchyme; secretes sonic hedgehog (SHH); establishes the anteroposterior (preaxial–postaxial, thumb–little finger) axis. Ectopic SHH → mirror-image duplication
Wnt7a / dorsal ectodermEstablishes the dorsoventral axis
Hox genesSpecify segment identity along the limb
Digit separationWeeks 6–8Interdigital apoptosis separates the digital rays. Failure → syndactyly
RotationWeeks 7–8Upper limb rotates laterally ~90°; lower limb rotates medially ~90° (Chapter 1)
OssificationFrom week 8Endochondral, from primary centres

Critical period: the limbs are most vulnerable to teratogens in weeks 4–8, which is exactly when thalidomide produced phocomelia and amelia.

Congenital conditions a physiotherapist will meet

ConditionDevelopmental basisPhysiotherapy relevance
Spina bifida (occulta, meningocele, myelomeningocele)Failure of caudal neuropore closure by day 28; folate-preventableLevel-dependent motor and sensory loss, neurogenic bladder and bowel, hydrocephalus, Chiari II; lifelong mobility, orthotic and skin-care management
Developmental dysplasia of the hip (DDH)Abnormal acetabular development and instability, influenced by intrauterine packing and postnatal positioningOrtolani and Barlow tests, Galeazzi sign, ultrasound screening; Pavlik harness; the swaddling posture matters — hips must be free to flex and abduct
Congenital talipes equinovarus (CTEV)Multifactorial; abnormal muscle and connective tissue developmentPonseti serial casting followed by bracing; physiotherapy in bracing adherence, stretching and gait
Torticollis (congenital muscular)Sternocleidomastoid fibrosis, often with a palpable massPositioning, stretching, active rotation, plagiocephaly management; screen for DDH, which co-occurs
Erb’s and Klumpke’s palsyTraction on the brachial plexus at birth — upper roots (C5–6) or lower (C8–T1)“Waiter’s tip” versus claw hand; positioning, range, sensory re-education, prevention of contracture and glenohumeral dysplasia
Arthrogryposis multiplex congenitaFetal akinesia from any cause → multiple congenital contracturesSerial casting, splinting, strengthening, long-term function
Cerebral palsyNon-progressive lesion of the developing brain (may be prenatal, perinatal or early postnatal)The largest paediatric neurological caseload in physiotherapy
Syndactyly / polydactylyFailed interdigital apoptosis / duplicated digital rayPost-surgical hand therapy
Osteogenesis imperfecta; achondroplasiaType I collagen defect; FGFR3 gain-of-function affecting the proliferative zoneSafe strengthening, mobility, fracture prevention (Chapter 2)

Where students consistently go wrong

  • Forgetting the stratum lucidum is only in thick skin.
  • Thinking skin colour reflects melanocyte number. It reflects melanin type, amount and distribution.
  • Assuming scar regains normal strength. It plateaus at 70–80% and lacks appendages and elasticity.
  • Missing the deep-partial burn. Reduced sensation and blotchy non-blanching appearance means likely grafting and near-certain hypertrophic scarring.
  • Positioning the burned patient comfortably. The comfortable position is the contracture position; use the anti-deformity position.
  • Underestimating a pressure injury. Muscle dies before skin; the visible lesion is the tip.
  • Using thermal agents over insensate skin. A persistent and avoidable source of harm.
  • Confusing dermatome, myotome and sclerotome. Skin, muscle and bone from the same somite and root.
  • Treating dermatome maps as exact. Adjacent dermatomes overlap substantially.
  • Forgetting the diaphragm’s cervical origin. C3–C5 explains shoulder-tip pain and, more importantly, why a lesion above C3 abolishes spontaneous ventilation.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Q1. The layer of epidermis containing the mitotic cells is
  1. (A) stratum corneum
  2. (B) stratum granulosum
  3. (C) stratum basale
  4. (D) stratum lucidum

Answer: (C) It also houses melanocytes and Merkel cells.

Q2. Melanocytes are derived from
  1. (A) mesoderm
  2. (B) endoderm
  3. (C) neural crest
  4. (D) surface ectoderm alone

Answer: (C) Which is why pigmentary and neurological anomalies co-occur in neurocristopathies.

Q3. Eccrine sweat glands are innervated by
  1. (A) sympathetic adrenergic fibres
  2. (B) sympathetic cholinergic fibres
  3. (C) parasympathetic fibres
  4. (D) somatic efferents

Answer: (B) The classic exception to sympathetic adrenergic transmission.

Q4. The key orchestrating cell of wound healing is the
  1. (A) neutrophil
  2. (B) macrophage
  3. (C) mast cell
  4. (D) platelet

Answer: (B) It arrives at 48–72 hours and coordinates debridement and the proliferative phase.

Q5. At six weeks, a healing wound has approximately what proportion of final tensile strength?
  1. (A) 5%
  2. (B) 20%
  3. (C) 50–60%
  4. (D) 100%

Answer: (C) Remodelling continues for a year or more, plateauing at 70–80% of original.

Q6. A keloid differs from a hypertrophic scar in that it
  1. (A) remains within the wound boundary
  2. (B) extends beyond the original wound margin
  3. (C) always regresses
  4. (D) never recurs after excision

Answer: (B)

Q7. A burn that is blotchy red and white, does not blanch well, and has reduced sensation is
  1. (A) superficial
  2. (B) superficial partial thickness
  3. (C) deep partial thickness
  4. (D) full thickness

Answer: (C) It usually requires grafting and scars hypertrophically.

Q8. A pressure injury with non-blanchable erythema and intact skin is stage
  1. (A) 1
  2. (B) 2
  3. (C) 3
  4. (D) unstageable

Answer: (A)

Q9. Sclerotome gives rise to
  1. (A) skeletal muscle
  2. (B) dermis of the back
  3. (C) vertebrae and ribs
  4. (D) spinal cord

Answer: (C)

Q10. The deep muscles of the back are derived from the epimere and innervated by
  1. (A) ventral rami
  2. (B) dorsal rami
  3. (C) the sympathetic chain
  4. (D) cranial nerves

Answer: (B) All other skeletal muscle derives from the hypomere and is supplied by ventral rami.

Q11. Referred pain to the tip of the shoulder from diaphragmatic irritation is explained by
  1. (A) direct nerve compression
  2. (B) the diaphragm’s cervical origin, retaining C3–C5 innervation via the phrenic nerve
  3. (C) the axillary nerve
  4. (D) trapezius spasm

Answer: (B)

Q12. The apical ectodermal ridge controls
  1. (A) anteroposterior axis
  2. (B) dorsoventral axis
  3. (C) proximodistal outgrowth
  4. (D) digit apoptosis

Answer: (C) The ZPA (via SHH) sets the anteroposterior axis.

Q13. Syndactyly results from failure of
  1. (A) limb bud formation
  2. (B) interdigital apoptosis
  3. (C) limb rotation
  4. (D) neural crest migration

Answer: (B)

Q14. The critical period for limb teratogenesis is
  1. (A) weeks 1–2
  2. (B) weeks 4–8
  3. (C) weeks 12–16
  4. (D) the third trimester

Answer: (B) The thalidomide window.

Q15. Which germ layer gives rise to the adrenal medulla?
  1. (A) Endoderm
  2. (B) Intermediate mesoderm
  3. (C) Neural crest
  4. (D) Lateral plate mesoderm

Answer: (C) The adrenal cortex, by contrast, is mesodermal — two different origins in one gland.

Quick review

Everything on this page, in one screen

  • Skin:
  • Epidermis (ectoderm, avascular, stratified squamous keratinised): basale → spinosum → granulosum → lucidum (thick skin only) → corneum. Turnover ~28–40 days. Non-keratinocytes: melanocyte and Merkel (neural crest), Langerhans (marrow)
  • Dermis (mesoderm): papillary (Meissner, capillary loops) and reticular (dense irregular, Pacinian, Ruffini, appendages). Langer’s lines determine scar quality
  • Eccrine sweat glands are sympathetic cholinergic and thermoregulatory; apocrine are pubertal and follicle-associated; sebaceous are holocrine
  • Skin blood flow ranges 0.5–30% of cardiac output. Never use thermal agents over insensate or ischaemic skin
  • Wound healing: haemostasis → inflammation (macrophage is the key cell) → proliferation (type III, granulation, epithelialisation, contraction) → remodelling (3 weeks to 1–2 years). Strength: 20% at 3 weeks, 50–60% at 6 weeks, 70–80% final
  • Hypertrophic stays within the wound; keloid extends beyond. Manage with pressure, silicone, massage, sustained stretch and splinting during remodelling
  • Burns: superficial · superficial partial (painful, blanching) · deep partial (reduced sensation, blotchy — grafts and hypertrophic scar) · full thickness (insensate, leathery). Rule of nines. Anti-deformity positioning is the opposite of comfortable positioning
  • Pressure injury: pressure + shear + moisture + friction; deeper than it appears; stages 1–4, unstageable, deep tissue injury. Prevention (repositioning, seating, pressure relief, transfer technique) is the physiotherapy contribution
  • Development:
  • Week 2 bilaminar, week 3 gastrulation → three germ layers, weeks 3–4 neurulation
  • Ectoderm → epidermis and appendages + neural tube (CNS) + neural crest (DRG, Schwann cells, adrenal medulla, melanocytes, enteric ganglia, facial skeleton)
  • Mesoderm → paraxial (somites: sclerotome/myotome/dermatome), intermediate (urogenital), lateral plate (limbs, body wall, heart, vessels, blood)
  • Endoderm → gut and respiratory epithelium, liver, pancreas, thyroid, thymus, bladder epithelium
  • Somites: 42–44 pairs; each retains its own spinal nerve however far it migrates — the basis of dermatome, myotome, sclerotome, viscerotome. Epimere → dorsal rami; hypomere → ventral rami
  • Dermatomes overlap; single-root section rarely produces a clear anaesthetic patch. Learn the reliable key points
  • Referred pain by convergence–projection: heart → T1–T5 left arm; central diaphragm → C3–C5 shoulder tip (because it forms in the neck and migrates); gallbladder → right scapula; ureter → loin to groin; testis/ovary → T10 periumbilical; hip → knee via obturator
  • Limb development weeks 4–8 (the teratogenic window): AER = proximodistal, ZPA/SHH = anteroposterior, Wnt7a = dorsoventral; interdigital apoptosis separates digits; upper limb rotates laterally 90°, lower limb medially 90°
  • Congenital conditions to recognise: spina bifida, DDH, CTEV, torticollis, Erb’s and Klumpke’s palsy, arthrogryposis, cerebral palsy, syndactyly

Further reading

SourceWhy it earns its place
Standring S (ed.) — Gray’s Anatomy, 42nd ednReference account of skin and of development, integrated by region
Sadler TW — Langman’s Medical EmbryologyThe standard student embryology text; the clearest treatment of somites, germ layers and limb development
Moore KL, Persaud TVN, Torchia MG — The Developing Human: Clinically Oriented EmbryologyStronger on clinical correlation and congenital anomaly
Ross MH, Pawlina W — Histology: A Text and AtlasEpidermal layers, appendages and cutaneous receptors
Sussman C, Bates-Jensen BM — Wound Care: A Collaborative Practice Manual for Health ProfessionalsThe physiotherapy-facing reference for wound and scar management
EPUAP/NPIAP/PPPIA — Prevention and Treatment of Pressure Ulcers/Injuries: Clinical Practice Guideline (2019)The current international staging and prevention standard
Procter F — “Rehabilitation of the burn patient”, Indian J Plast Surg, 2010Anti-deformity positioning and burn rehabilitation, in an Indian context
Lee Dellon A; and Lee MWL, McPhee RW, Stringer MD — “An evidence-based approach to human dermatomes”, Clin Anat, 2008The evidence on dermatome variability and overlap
ASIA — International Standards for Neurological Classification of Spinal Cord InjuryThe key sensory and motor points you will actually use
Palastanga N, Field D, Soames R — Anatomy and Human MovementThe physiotherapy-facing synthesis

Chapter 8 of 24 · Human Anatomy · Physiotherapist India End of Part 1 — General anatomy. Next: Chapter 9 — Bones of the Upper Limb, opening Part 2.

Reviewed by the Physiotherapist India Team. · Human Anatomy contents