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
Anterior
compartment

Tibialis anterior, extensor hallucis

longus, extensor digitorum longus and
peroneus tertius

Neurovascular Structures
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
Medial

Abductor hallucis, flexor hallucis brevis

Lateral

Abductor digiti minimi, flexus digiti minimi brevis

Neurovascular Structures

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.