Muscles

These five muscles have nothing to do with moving the spine — they all act on the upper limb and are called “extrinsic” because they migrated onto the back from limb-bud territory during development. That embryological origin explains their nerve supply: trapezius is innervated by CN XI (a cranial nerve!) because it derives from branchial arch mesenchyme, not from spinal muscle. Latissimus dorsi is the great climbing and swimming muscle — it pulls the arm forcefully downward and backward, which is exactly what you do when hauling yourself out of a swimming pool. The clinical analogy that unifies this group: think of each muscle as a rope connecting one body part to another; when the rope is cut (nerve injury), the structure it was holding drifts away.

The intrinsic back muscles are the true movers and stabilisers of the vertebral column. Think of the erector spinae as three parallel columns of cables running the entire length of the spine: when they shorten symmetrically they pull the column into extension (straightening up from a forward bend); when they shorten on one side they produce lateral flexion. The multifidus sits even deeper, spanning only 2–4 vertebral levels, and acts as a fine-tuning stabiliser rather than a gross mover — it is the muscle that rehabilitation programmes target in chronic low back pain, because it is selectively inhibited and atrophies after a back injury while the superficial erectors compensate. Both groups are supplied by the posterior rami of spinal nerves, which is why they are anatomically and embryologically separate from the anterior abdominal musculature.

Erector spinae (lateral to medial): Iliocostalis (ribs), Longissimus (transverse processes), Spinalis (spinous processes). Supplied by posterior rami of spinal nerves. Actions: extension and lateral flexion of the vertebral column; maintain upright posture.

Multifidus: deep to erector spinae; spans 2–4 vertebrae; most powerful rotator/stabiliser of the spine; important in low back pain rehabilitation.

You take roughly 20,000 breaths a day, and for each quiet breath the diaphragm does virtually all the work. Think of it as a piston: when its muscle fibres contract, the central tendon descends like the bottom of a syringe being pulled, expanding the thoracic volume and drawing air in. It then relaxes passively and recoils upward as the lungs' elastic recoil drives expiration. The genius of the design is the three holes in it — each at a different level, each transmitting different structures. Remembering these three levels is non-negotiable for any anatomy or surgical exam: T8 IVC, T10 oesophagus, T12 aorta (“I 8 ten eggs at 12”). The phrenic nerve originates from C3–C5, which is why diaphragm irritation (blood under the diaphragm, sub-phrenic abscess) refers pain to the tip of the shoulder — both are C4 dermatomal territory.

Nerve supply: Phrenic nerve C3, C4, C5 — "C3, 4, 5 keeps the diaphragm alive". Peripheral: lower 5 intercostal nerves (sensory only). Referred pain from diaphragm: C4 dermatome = tip of shoulder.

The three layers of intercostal muscle mimic the three layers of the abdominal wall — external, internal, innermost — and their fibre directions alternate in the same way. The external intercostals run like your fingers in your pockets (“hands in pockets” = inferomedial): they pull the ribs up and apart during inspiration. The internal layer runs the opposite way and is active during forced expiration. The crucial practical point is where the neurovascular bundle runs: it is tucked under the rib in the costal groove, and it runs vein–artery–nerve from top to bottom (“VAN”). Insert a needle or drain just above the upper border of the rib below to stay clear of it.

The inguinal canal is an engineering problem: the abdominal wall needs to be airtight to resist the pressure surges of coughing, straining, and lifting, yet it must also allow the spermatic cord (in males) or the round ligament (in females) to pass through. The solution is an oblique tunnel, not a straight hole. By running diagonally through the wall for ~4 cm, the canal creates a natural flap-valve mechanism — when intra-abdominal pressure rises, the canal walls are compressed together rather than blown open. Where this mechanism fails, a hernia forms. The key to distinguishing hernia types is the relationship to the inferior epigastric vessels: indirect hernias pass lateral to these vessels (through the deep ring), while direct hernias bulge medially through the posterior wall of the canal. Think “MD — Medial Direct.” The clinical examination test (press over the deep ring and ask the patient to cough) exploits this anatomy.

The forearm is divided into two compartments by the interosseous membrane: the anterior (flexor) compartment bends the wrist and fingers and pronates the forearm; the posterior (extensor) compartment does the opposite. The nerve that controls each compartment matches its name: the median nerve (with its deep branch, the anterior interosseous nerve) runs anteriorly and supplies most flexors, while the radial nerve (specifically its posterior interosseous nerve) supplies the extensor compartment. The single important exception to this clean divide is the flexor carpi ulnaris and the medial half of flexor digitorum profundus — these anterior muscles are supplied by the ulnar nerve, not the median. This exception matters enormously in nerve injury: in a high ulnar nerve lesion, the patient cannot flex the DIP joints of the ring and little fingers, which paradoxically reduces the severity of the ulnar claw (the “ulnar paradox”).

The intrinsic hand muscles are what make the human hand unique — they allow the precision grip and fine manipulation that no other primate can replicate. Almost all of them are supplied by the ulnar nerve, with the critical exception of the LOAF muscles (supplied by the median nerve's recurrent branch). The lumbricals have a peculiar and beautiful action: they flex the MCP joint while simultaneously extending the PIP and DIP joints — the exact position needed to hold a pen. They can do this because they originate from the flexor digitorum profundus tendons (so they are flexors of MCP) and insert into the extensor expansion (so they extend the IPs). When the ulnar nerve is cut, the ring and little finger lumbricals (L3 and L4) are lost, producing clawing at those fingers: MCP hyperextends because the lumbricals no longer resist it, while the IPs flex because FDP is intact but unopposed by the extensor expansion mechanism.

Carpal tunnel syndrome is the most common peripheral nerve entrapment, and its presentation follows directly from the anatomy: the median nerve is compressed in a rigid fibro-osseous channel and has nowhere to go. The classic symptom of nocturnal tingling is explained by fluid redistribution when the hand hangs dependently during sleep — venous engorgement within the tunnel raises the pressure further. The first muscle that wastes is abductor pollicis brevis (LOAF mnemonic, recurrent branch of median nerve), which is why you examine the thenar eminence in every patient with hand symptoms. The clinical tests work by reproducing the compression: Phalen's test maximally flexes the wrist (closes the tunnel), while Durkan's test applies direct pressure. Importantly, ulnar nerve sensation is preserved in CTS — if the little finger is numb, look for a more proximal lesion or ulnar nerve pathology at Guyon's canal.

Volkmann's contracture is compartment syndrome’s most feared legacy in the forearm. The anterior compartment contains the deep flexors (FDP, FPL) which are the muscles most vulnerable to ischaemia because they are farthest from the fascial surface and therefore the last to receive blood when pressure rises. When these muscles die and are replaced by fibrous scar, they shorten — pulling the wrist into flexion, the fingers into an IP-flexed, MCP-extended claw. The pathognomonic clinical test is passive wrist extension: extending the wrist takes up slack in the long flexors and forces the fingers into tighter flexion, confirming that the contracture is in the muscle/tendon, not intrinsic to the finger joints. The lesson is always prevention: any swelling of the forearm after a supracondylar fracture is a compartment syndrome until proved otherwise, and a rising pressure >30 mmHg or within 30 mmHg of diastolic mandates immediate fasciotomy.

Gluteus maximus is the most powerful extensor in the body — it is what drives you up a staircase, out of a deep chair, or off the starting block. Gluteus medius and minimus are the abductors, and they do something even more essential during walking: every time you lift one foot off the ground, the gluteus medius of the stance leg must fire to stop the pelvis from dropping toward the unsupported side. This is the Trendelenburg mechanism, and it explains one of the most clinically important signs in musculoskeletal medicine. The piriformis is important for a different reason: it passes directly over the sciatic nerve, and in a small percentage of people the nerve actually passes through the muscle — this is piriformis syndrome, a cause of sciatica with a normal MRI spine. The gluteal region is also where the superior gluteal nerve (to gluteus medius/minimus) must not be injured during intramuscular injections, which is why the upper outer quadrant of the buttock is used.

The thigh has three compartments with completely different roles. The anterior compartment (quadriceps + iliopsoas) is the stair-climbing, kicking, standing-from-sitting engine of the lower limb — supplied by the femoral nerve. The medial compartment (adductors) pulls the limb toward the midline during running and provides pelvic stability; it is largely supplied by the obturator nerve (L2–L4). The posterior compartment (hamstrings) is unique because all three muscles cross both the hip and knee: they extend the hip in activities like sprinting and running upstairs, and they flex the knee. The hamstrings are the most commonly torn muscles in sport, usually at or near their origin at the ischial tuberosity during explosive sprinting (the “pop” felt in the back of the thigh). Knowing that the short head of biceps femoris is not a true hamstring (it does not cross the hip and is supplied by the common peroneal division, not the tibial division) is a favourite exam distinction.

All muscles of facial expression share two characteristics: they are inserted into skin (not bone-to-bone), and they are all innervated by the facial nerve (CN VII). They develop from the 2nd pharyngeal arch, which is why CN VII — the 2nd arch nerve — supplies them all. The high-yield clinical principle is the UMN vs LMN distinction: the frontalis (forehead) muscle receives bilateral cortical input, so a unilateral stroke (UMN lesion) spares it — the patient can still wrinkle their forehead even though the lower face is weak. In Bell’s palsy (LMN lesion of CN VII itself), the entire ipsilateral face fails including the forehead. This single observation — can the patient wrinkle their brow? — immediately tells you whether the lesion is above or below the level of the facial nerve nucleus in the pons.

The four muscles of mastication all move the mandible and are all supplied by the mandibular division of the trigeminal nerve (CN V3) — because they develop from the 1st pharyngeal arch. Think of them in two functional pairs: jaw closers (masseter + temporalis + medial pterygoid) and one jaw opener (lateral pterygoid — its inferior head depresses the mandible by pulling the condyle and disc anteriorly). The masseter is the most powerful jaw-closer by cross-sectional area; you can feel it bulk up when you clench your teeth. The lateral pterygoid is the only muscle that opens the jaw actively — gravity and digastric assist — which is why a unilateral lateral pterygoid contraction deflects the chin to the opposite side. In trigeminal neuralgia, intense lancinating pain is triggered by chewing, making these muscles clinically important even when structurally intact.

The sternocleidomastoid (SCM) is the dominant strap of the anterior neck. When both contract together they flex the cervical spine and extend the head at the atlanto-occipital joint (chin protrudes forward, not down — an important distinction). When one contracts alone it tilts the ear toward the ipsilateral shoulder and rotates the chin to the opposite side — the clinical rule is: the muscle turns the face away from itself. SCM receives a dual nerve supply from CN XI (spinal accessory) for movement and C2–C3 for proprioception; this dual supply means that testing SCM with resistance tests CN XI function, making it a simple bedside test for accessory nerve integrity after posterior triangle neck surgery. The scalene muscles are more than just neck flexors: the gap between anterior and middle scalenes (the interscalene triangle) is the exit route for the brachial plexus roots and subclavian artery, making scalene hypertrophy or a cervical rib a cause of thoracic outlet syndrome.

Fig. 8.17 — Anterior and posterior triangles of the neck

Gray's Anatomy for Students, 4e

Note how SCM forms the common boundary between both triangles

Neck muscles — SCM, Trapezius, ansa cervicalis (C1–C3) to strap muscles, and brachial plexus exit

Gray's Anatomy for Students, 4e

Ansa cervicalis (green) — C1 descends with CN XII then loops with C2–C3 to supply all strap muscles

Fig. 8.12 — Key vertebral levels: CIII–CIV (carotid bifurcation), CV–CVI (cricoid / trachea start)

Gray's Anatomy for Students, 4e

Clinically vital for neck palpation, carotid endarterectomy, and tracheostomy landmarks

The suprahyoid muscles sit above the hyoid bone and form the muscular floor of the mouth. Their collective job is to move the hyoid and tongue during swallowing: when the hyoid is fixed by the infrahyoid muscles, the suprahyoids open the jaw; when the jaw is fixed, they elevate the hyoid and larynx — the upward jerk you can feel under your chin when you swallow is these muscles contracting. The mylohyoid forms a true diaphragm (the oral diaphragm), its right and left halves meeting at a midline raphe; abscesses in the floor of the mouth can spread either above or below it, changing both the clinical presentation and the drainage approach. The digastric has a fascinating dual nerve supply: its anterior belly is a 1st arch muscle (V3) and its posterior belly is a 2nd arch muscle (CN VII) — the intermediate tendon connecting them passes through a fibrous loop anchored to the hyoid, making it the only muscle with a pulley system in the neck.

Fig. 8.13 — Larynx and neck strap muscles: sternohyoid, omohyoid, thyroid gland

Gray's Anatomy for Students, 4e

Sternohyoid is superficial; omohyoid crosses obliquely — both depressed by ansa cervicalis

The soft palate separates the oral cavity from the nasopharynx. During swallowing it must rise and seal against the posterior pharyngeal wall to prevent food entering the nose — a failure here causes nasal regurgitation. Its five muscles are controlled almost entirely by the vagus nerve (CN X) via the pharyngeal plexus, with one critical exception: tensor veli palatini is innervated by V3 (medial pterygoid branch). Tensor has a unique job beyond palate stiffening — its tendon hooks around the pterygoid hamulus and fans out to open the cartilaginous Eustachian tube with each swallow and yawn. This is why children with cleft palate have chronic middle ear effusions ("glue ear"): the abnormal tensor cannot open the Eustachian tube properly. The palatoglossus is the one muscle in this group not innervated by CN XII despite having "glossus" in its name — it too is CN X, a classic exam trap.

Fig. 8.10 — Soft palate: A. Position (nasopharynx / oropharynx / laryngopharynx), B. Muscle layer

Gray's Anatomy for Students, 4e

Levator veli palatini elevates to seal the nasopharynx — failure → nasal regurgitation

All soft palate muscles are supplied by the vagus nerve (CN X) via the pharyngeal plexus, EXCEPT tensor veli palatini (CN V3).

If you removed the pelvis and looked up from below, you would see the pelvic floor as a hammock of muscle spanning the bony ring, pierced by three openings: the urethra, vagina (in females), and anal canal. This hammock — the pelvic diaphragm — consists primarily of levator ani, a broad sheet with three named parts (pubococcygeus, puborectalis, iliococcygeus), plus coccygeus posteriorly. The critical part is puborectalis: its U-shaped sling wraps behind the anorectal junction, creating the anorectal angle of roughly 90°. Faecal continence depends on this angle — the kink means that any increase in intra-abdominal pressure (coughing, straining) compresses the anorectal junction closed rather than forcing it open. During defecation, puborectalis relaxes and the angle straightens to 135°, allowing passage. Damage to puborectalis from obstetric injury or pudendal neuropathy abolishes this angle and causes faecal incontinence even with intact sphincters.

The perineum is the diamond-shaped region below the pelvic diaphragm. A transverse line between the two ischial tuberosities divides it into the urogenital triangle anteriorly (urethra and vagina/penis) and the anal triangle posteriorly. The perineal body (central tendon of the perineum) is the fibromuscular knot at the centre of this region where eight muscles converge; it is the anchor that holds the perineum together. Obstetric tears are graded by how far back through this region they extend: a 4th-degree tear reaches the internal anal sphincter and requires careful surgical layered repair. The external urethral sphincter is skeletal muscle under voluntary pudendal nerve control — this is why a spinal cord injury at or above S2 causes spastic retention (sphincter cannot relax), while a lower motor neuron lesion causes stress incontinence (sphincter cannot contract). Ischiocavernosus and bulbospongiosus drive erection and ejaculation by compressing the venous outflow of the corpora — pudendal nerve anaesthetic block for perineal surgery will temporarily abolish these reflexes.