Compartments of the Thigh

Compartment Muscles Neurovascular Structures

Anterior compartment

sartorius muscle and the four quadriceps the rectus femoris, vastus lateralis, vastus intermedius vastus medialis and the articularis genus

femoral nerve

Medial compartment

pectineus, external obturator, and the gracilis muscles, together with the four adductors the longus, brevis, magnus and minimus

obturator nerve

Posterior compartment

biceps femoris, semitendinosus and semimembranosus muscles sciatic nerve

Compartments of the Leg

Compartment Muscles Neurovascular Structures

Anterior compartment

Tibialis anterior, extensor hallucis longus, extensor digitorum longus and peroneus tertius

Deep fibular nerve andanterior tibial vessels

Lateral compartment

Fibularis longus and brevis Superficial fibular nerve

Deep posterior compartment

Tibialis posterior, flexor hallucis longus, flexor digitorum longus and Popliteus

Tibial nerve, posterior tibial artery and posterior tibial vessels such as the fibular artery

Superficial posterior compartment

Gastrocnemius, soleus and plantaris Medial sural cutaneous nerve

Compartments of the Foot

Compartment Muscles Neurovascular Structures

Medial Abductor hallucis, flexor hallucis brevis

Lateral Abductor digiti minimi, flexus digiti minimi brevis

Interosseous (4x) Intrinsic muscles between the 1st and 5th metatarsals

Superficial central Flexor digitorum brevis

Central Quadratus plantae

Deep central Adductor hallucis posterior tibial neurovascular bundle

An upper motor neuron lesion (also known as pyramidal insufficiency) is a lesion of the neural pathway above the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves. This is in contrast to a lower motor neuron lesion, which affects nerve fibers traveling from the anterior horn of the spinal cord or the cranial motor nuclei to the relevant muscle(s). One major characteristic used to identify a lower motor neuron lesion is flaccid paralysis paralysis accompanied by loss of muscle tone. This is in contrast to an upper motor neuron lesion, which often presents with spastic paralysis paralysis accompanied by severe hypertonia.

Neuromuscular-blocking drugs block neuromuscular transmission at the neuromuscular junction, causing paralysis of the affectedskeletal muscles. This is accomplished either by acting presynaptically via the inhibition of acetylcholine (ACh) synthesis or release or by acting postsynaptically at the acetylcholine receptors of the motor nerve end-plate. While some drugs act presynaptically (such as botulinum toxin and tetanus toxin), those of current clinical importance work postsynaptically.

These drugs fall into two groups: Non-depolarizing blocking agents: These agents constitute the majority of the clinically relevant

neuromuscular blockers. They act by competitively blocking the binding of ACh to its receptors, and in some cases, they also directly block the ionotropic activity of the ACh receptors.

Depolarizing blocking agents: These agents act by depolarizing the sarcolemma of the skeletal muscle fiber. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh.

The main difference is in the reversal of these two types of neuromuscular-blocking drugs. Non-depolarizing blockers are reversed by acetylcholinesterase inhibitor drugs since they are

competitive antagonists at the ACh receptor so can be reversed by increases in ACh. The depolarizing blockers already have ACh-like actions, so these agents have prolonged effect under the

influence of acetylcholinesterase inhibitors. Administration of depolarizing blockers initially produces fasciculations (a sudden twitch just before paralysis occurs). This is due to depolarization of the muscle. Also, post-operative pain is associated with depolarizing blockers.

Non-depolarizing agents A decrease in binding of acetylcholine leads to a decrease in its effect

and neuron transmission to the muscle is less likely to occur. It is generally accepted that non-depolarizing

agents block by acting as reversible competitive inhibitors. That is, they bind to the receptor

as antagonists and that leaves fewer receptors available for acetylcholine to bind. Depolarizing agents Depolarizing agents produce their block by binding to and activating the ACh receptor, at first causing muscle contraction, then paralysis. They bind to the receptor and cause depolarization by opening channels just like acetylcholine does. This causes repetitive excitation that lasts longer than a normal acetylcholine excitation and is most likely explained by the resistance of depolarizing agents to the enzyme acetylcholinesterase. The constant depolarization and triggering of the receptors keeps the endplate resistant to activation by acetylcholine. Therefore a normal neuron transmission to muscle cannot cause contraction of the muscle because the endplate is depolarized and thereby the muscle paralysed.