Brachial plexus

Brachial plexus

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The brachial plexus is a network of nerves formed by the anterior rami of C5-T1. It supplies motor and sensory innervation to most of the upper limb.

Order of components

Roots → Trunks → Divisions → Cords → Branches

Mnemonic: “Read That Damn Cadaver Book”

Part	Arrangement
Roots	C5, C6, C7, C8, T1
Trunks	Upper: C5-C6; Middle: C7; Lower: C8-T1
Divisions	Each trunk splits into anterior and posterior divisions
Cords	Lateral, posterior, medial, named by relation to the axillary artery
Terminal branches	Musculocutaneous, Axillary, Radial, Median, Ulnar

Formation of the cords

Lateral cord: anterior divisions of upper and middle trunks
Medial cord: anterior division of lower trunk
Posterior cord: all three posterior divisions

Five terminal nerves

Nerve	Main root values	Key function
Musculocutaneous	C5-C7	Flexors of arm, especially biceps; sensation over lateral forearm
Axillary	C5-C6	Deltoid and teres minor; sensation over lateral shoulder
Radial	C5-T1	Extensors of arm and forearm; sensation over posterior limb and dorsolateral hand
Median	C6-T1	Most forearm flexors, thenar muscles; sensation over lateral palm and lateral 3½ digits
Ulnar	C8-T1	Most intrinsic hand muscles; sensation over medial 1½ digits

Important collateral branches

From roots: dorsal scapular nerve (C5), long thoracic nerve (C5-C7)
From upper trunk: suprascapular nerve, nerve to subclavius
From lateral cord: lateral pectoral nerve
From medial cord: medial pectoral, medial cutaneous nerve of arm and forearm
From posterior cord: upper and lower subscapular nerves, thoracodorsal nerve

Clinical correlations

Upper trunk injury, C5-C6: Erb palsy, classically “waiter’s tip” posture.
Lower trunk injury, C8-T1: Klumpke palsy, weakness of intrinsic hand muscles, possibly clawing.
Long thoracic nerve injury: winged scapula due to serratus anterior paralysis.
Posterior cord lesion: may affect axillary and radial nerve functions.

The plexus begins in the neck, passes between the anterior and middle scalene muscles, crosses over the first rib, and enters the axilla where its cords surround the axillary artery. Gray’s Anatomy for Students, p. 858. A concise NCBI anatomy review also summarizes the roots-to-terminal-branches sequence.

Explain brachial plexus lesions by clinical presentation

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Brachial plexus lesions cause patchy weakness, sensory loss, and reduced reflexes that do not fit one single root or peripheral nerve. The clinical pattern helps localize the lesion.

1. Upper plexus lesion: C5-C6, sometimes C7

Also called Erb palsy or upper-trunk palsy

Typical mechanism

Traction separating the head and shoulder, such as a fall on the shoulder, motorcycle injury, or shoulder dystocia at birth.

Clinical presentation

Weak shoulder abduction and external rotation: deltoid, supraspinatus, infraspinatus
Weak elbow flexion and supination: biceps, brachialis
In more extensive lesions, weak wrist and finger extension
Reduced or absent biceps reflex and often brachioradialis reflex
Sensory loss over the lateral shoulder and lateral arm/forearm, in a C5-C6 pattern

Typical posture in severe neonatal Erb palsy

Arm adducted and internally rotated
Elbow extended
Forearm pronated
Known as the “waiter’s tip” posture

Key clue: proximal arm weakness predominates, especially deltoid and biceps.

2. Lower plexus lesion: C8-T1

Also called Klumpke palsy or lower-trunk palsy

Typical mechanism

Violent upward traction of an abducted arm, for example grasping something while falling
Compression at the thoracic outlet
Apical lung tumor, particularly a Pancoast tumor

Clinical presentation

Marked weakness and wasting of intrinsic hand muscles
Weak finger abduction/adduction and impaired fine finger movements
Weak grip
May also weaken finger and wrist flexion
Sensory loss or pain along the medial forearm, medial hand, and little finger, roughly C8-T1/ulnar-sided distribution
Reduced or absent grasp reflex in neonates

Associated Horner syndrome

Ptosis, miosis, and facial anhidrosis suggest involvement of T1 sympathetic fibers, often indicating a lower-root avulsion or Pancoast tumor.

Key clue: hand weakness and medial-arm sensory symptoms predominate.

3. Total brachial plexus lesion: C5-T1

Typical mechanism

Major traction injury, high-energy trauma, severe birth trauma, or extensive tumor/infiltrative disease.

Clinical presentation

Flaccid, weak or completely paralysed upper limb
Loss of shoulder, elbow, wrist, and hand movements
Widespread sensory loss in the limb
All relevant upper-limb reflexes may be absent
Severe neuropathic pain may occur
If lower roots are avulsed, Horner syndrome may coexist

Key clue: near-complete motor and sensory loss in one upper limb.

4. Posterior cord lesion

The posterior cord supplies the axillary and radial nerves.

Clinical presentation

Weak shoulder abduction from deltoid weakness
Weak elbow, wrist, and finger extension due to radial involvement
Wrist drop
Sensory loss over the lateral shoulder and posterior arm/forearm, extending to the dorsolateral hand

Key clue: combination of deltoid weakness plus wrist/finger extensor weakness.

5. Lateral cord lesion

The lateral cord contributes to the musculocutaneous nerve and lateral part of the median nerve.

Clinical presentation

Weak elbow flexion and forearm supination from musculocutaneous involvement
Reduced biceps reflex
Sensory loss over lateral forearm
May have variable median-nerve-pattern weakness in the forearm/hand

Key clue: biceps weakness with lateral forearm sensory loss, often broader than an isolated musculocutaneous neuropathy.

6. Medial cord lesion

The medial cord contributes to the ulnar nerve, medial median contribution, and medial cutaneous nerves.

Clinical presentation

Weak intrinsic hand muscles
Weakness in ulnar- and median-innervated hand muscles
Sensory loss over medial arm, medial forearm, and ulnar side of hand
May mimic ulnar neuropathy, but medial forearm sensory loss and median-intrinsic hand involvement indicate a more proximal lesion

Key clue: lower-plexus pattern with medial arm/forearm sensory involvement.

7. Root avulsion: preganglionic lesion

A root is torn from the spinal cord, usually in high-energy traction trauma.

Clinical clues

Severe weakness, often profound
Neuropathic or burning pain
Horner syndrome, winged scapula, weak rhomboids, or elevated hemidiaphragm support a proximal/root-level lesion
Sensation may be clinically impaired but sensory nerve action potentials can remain preserved on nerve-conduction testing because the dorsal root ganglion remains connected to the peripheral sensory nerve
EMG may show denervation in paraspinal muscles

These lesions have a worse prognosis than postganglionic plexus injuries. Miller’s Review of Orthopaedics, pp. 697-698.

8. Nontraumatic brachial plexopathy patterns

Cause	Characteristic presentation
Parsonage-Turner syndrome or neuralgic amyotrophy	Sudden, severe shoulder or supraclavicular pain followed days later by weakness and atrophy, often involving upper-trunk muscles or serratus anterior. Sensory loss is usually mild.
Neoplastic plexopathy	Severe, progressive pain followed by weakness, atrophy, and sensory loss. Lower trunk/medial cord involvement is common. Pancoast tumor may produce C8-T1 symptoms plus Horner syndrome.
Radiation-induced plexopathy	Usually delayed, progressive, often relatively painless weakness and sensory symptoms after radiotherapy.
Thoracic outlet syndrome	Lower-trunk pattern: hand intrinsic weakness with sensory symptoms mainly in the ulnar distribution; symptoms may be posture-related.
Hematoma or mass compression	Acute or subacute painful mixed motor-sensory deficit, especially after trauma, vascular procedures, bleeding disorder, or anticoagulation.

A recent systematic review describes clinical assessment as requiring detailed mapping of weakness, reflexes, and sensory loss, with electrodiagnostic studies and imaging used to confirm localization when needed (2025 clinical assessment review).

Fast localization summary

Deltoid + biceps weak → upper trunk, C5-C6, Erb pattern
Intrinsic hand muscles weak → lower trunk, C8-T1, Klumpke pattern
Deltoid weakness + wrist drop → posterior cord
Whole limb flail → complete plexus lesion
Medial hand pain/weakness + Horner syndrome → lower trunk/T1 lesion, consider root avulsion or Pancoast tumor
Severe pain first, weakness later → Parsonage-Turner syndrome

New traumatic weakness, severe neuropathic pain, Horner syndrome, scapular winging, breathing difficulty, or suspected cervical root avulsion needs urgent specialist assessment.

Methyl alcohol posion and treatment

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Methanol (methyl alcohol, wood alcohol) poisoning

Methanol poisoning is a medical emergency. If ingestion is suspected, seek emergency care immediately and contact the local poison center. Do not wait for visual symptoms or laboratory confirmation before seeking help.

Sources

Methanol occurs in industrial solvents, windshield-washer fluid, and some “canned heat” products. It is metabolized as:

Methanol → formaldehyde → formic acid

Formic acid causes high-anion-gap metabolic acidosis, optic nerve/retinal toxicity, and central nervous system injury. Fomepizole or ethanol prevents formation of these toxic metabolites by inhibiting alcohol dehydrogenase. Katzung’s Basic and Clinical Pharmacology, 16th ed., p. 632.

Clinical presentation

There may be a latent symptom-free period of about 6-24 hours, longer if ethanol was co-ingested.

Stage	Features
Early	Inebriation, dizziness, headache, nausea, vomiting, abdominal pain
Progressive toxicity	Tachypnea from metabolic acidosis, confusion, drowsiness, hypotension
Characteristic toxicity	Blurred vision, photophobia, “snowfield” vision, reduced visual acuity, fixed/dilated pupils
Severe poisoning	Coma, seizures, respiratory failure, blindness, death

Important late complications include optic neuropathy and basal ganglia, especially putaminal, injury that can cause a Parkinsonian syndrome. Comprehensive Clinical Nephrology, 7th ed., Box 13.6.

Diagnosis

Suspect methanol toxicity in a patient with unexplained acidosis, visual symptoms, altered consciousness, or a history of solvent/windshield-fluid ingestion.

Typical investigations

Arterial or venous blood gas: metabolic acidosis, often severe
Serum electrolytes and bicarbonate
Anion gap: elevated
Measured and calculated serum osmolality: early osmolar gap may be elevated
Serum methanol concentration, if available
Renal function, glucose, lactate, ethanol concentration
ECG and continuous monitoring
CT/MRI brain if neurological complications are suspected

A normal osmolar gap does not exclude late poisoning because methanol may already have been converted to formate.

Treatment

1. Immediate resuscitation

Airway, breathing, circulation
Oxygen and ventilatory support if required
IV access, cardiac monitoring, serial neurologic and visual assessment
Consult a medical toxicologist/poison center and nephrology early.

2. Block toxic metabolism: fomepizole

Fomepizole is the preferred antidote.

A commonly used regimen:

15 mg/kg IV loading dose
Then 10 mg/kg IV every 12 hours for 48 hours
Then 15 mg/kg IV every 12 hours thereafter because of autoinduction
During intermittent hemodialysis, it must be given more frequently, often every 4 hours, according to the local protocol.

Do not delay antidotal treatment when suspicion is high, especially with acidosis, visual symptoms, elevated osmolar gap, or an available methanol level above the treatment threshold. Comprehensive Clinical Nephrology, 7th ed., Box 13.6.

3. If fomepizole is unavailable: ethanol

IV ethanol is an alternative because it competitively occupies alcohol dehydrogenase, reducing formate generation. It needs close monitoring because it can cause intoxication, hypoglycemia, and unstable blood ethanol concentrations. This should be administered only under a toxicology-directed hospital protocol.

4. Correct acidosis

Give IV sodium bicarbonate for significant metabolic acidosis.
This supports physiologic pH and reduces the proportion of undissociated formic acid that enters tissues.

5. Folate cofactor

Folinic acid (leucovorin) or folic acid is usually administered to enhance formate metabolism.
A common hospital regimen is folinic acid 50 mg IV every 4-6 hours, but follow local toxicology guidance.

6. Hemodialysis

Hemodialysis rapidly removes both methanol and formate and corrects acidosis. Intermittent hemodialysis is preferred when available.

The EXTRIP methanol recommendations recommend extracorporeal treatment when any of these are present:

Coma
Seizures
New visual deficit
pH ≤ 7.15
Persistent metabolic acidosis despite antidote and supportive treatment
Anion gap >24 mmol/L
Impaired renal function
High serum methanol concentration:
- 700 mg/L or 21.8 mmol/L while on fomepizole
- 600 mg/L or 18.7 mmol/L while on ethanol
- 500 mg/L or 15.6 mmol/L without an alcohol dehydrogenase blocker

Continue fomepizole or ethanol during dialysis, because dialysis also removes the antidote. Dialysis is generally stopped after clinical improvement and methanol falls below 200 mg/L (6.2 mmol/L), per EXTRIP.

Exam summary

Methanol poisoning

Toxic metabolite: formic acid
Main danger: high-anion-gap metabolic acidosis + visual loss
Antidote of choice: fomepizole
Additional treatment: sodium bicarbonate + folinic acid
Severe poisoning: hemodialysis
Classic visual symptom: “snowfield” vision

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