Severe brachial and facial muscle spasms

Went to sketchy tattoo parlor the day prior; fresh tattoo on shoulder

Facial spasms

Tetanus toxin has bonded to nerve endings; impossible to fully remove

Breathing impaired due to locked mandible and respiratory muscles (diaphragm, external/internal intercostals, etc.)

Clostridium tetani detected in blood samples; patient appears to have contracted generalized tetanus from unsterilized tattoo needles

Systems affected:


Muscular System:

  • Spasms, stiffness of muscles: jaw's Masseter muscle (trismus), neck and abdominal muscles
  • Painful body spasms lasting for several minutes; can be triggered by a draft, loud noise, light or physical touch

Circulatory System:

  • Fluctuations in blood pressure (higher/lower)
  • Rapid heart rate, cardiac arrhythmias

Skeletal System:

  • Severe muscle spasms may break surrounding bones
  • Any bones trapped within muscular spasms are not free to articulate as per usual

Nervous System:

  • Interferes with the signals traveling from the brain to the nerves in the spinal cord

Normal sequence of events at neuromuscular juntion (NMJ):


Each skeletal muscle fiber has one NMJ, innervated by a motor neuron. NMJs have a synaptic knob, motor end plate and synaptic cleft.


  1. A motor neuron releases acetylcholine (ACh) at the NMJ.


  2. ACh binds to receptors on the sarcolemma


  3. If enough ACh binds to receptors, an action potential is transmitted the full length of the muscle fiber


  4. The action potential triggers the release of Ca2+ from the sarcoplasmic reticulum


  5. Ca2+ binds to troponin on the actin filament, and the troponin pulls tropomyosin off the active sites, allowing myosin heads to attach to actin filament



Steps involved: Synaptic Vesicle Exocytosis


I . Trafficking: Vesicles are transported to the cell membrane along microtubules of the cytoskeleton. Movement of the vesicles is powered by the motor proteins kinesins, dyneins, and myosins.


II. Tethering: Upon reaching the cell membrane, the vesicle becomes linked to and pulled into contact with the cell membrane.


III. Docking: Involves the attachment of the vesicle membrane with the cell membrane. The phospholipid bilayers of the vesicle membrane and cell membrane begin to merge.


IV. Priming: Priming occurs in regulated exocytosis and not in constitutive exocytosis. This step involves specific modifications that must happen in certain cell membrane molecules for exocytosis to occur. These modifications are required for signaling processes that trigger exocytosis to take place.


V. Fusion: There are two types of fusion that can take place in exocytosis. In complete fusion, the vesicle membrane fully fuses with the cell membrane. The energy required to separate and fuse the lipid membranes comes from ATP. The fusion of the membranes creates a fusion pore, which allows the contents of the vesicle to be expelled as the vesicle becomes part of the cell membrane. In kiss-and-run fusion, the vesicle temporarily fuses with the cell membrane long enough to create a fusion pore and release its contents to the exterior of the cell. The vesicle then pulls away from the cell membrane and reforms before returning to the interior of the cell.

Difference between a twitch, a summation and tetany:


When the muscle is stimulated with a single electric shock of sufficient voltage, it quickly contracts and relaxes. This response is called a twitch.


If a second electric shock is delivered immediately after the first, it will produce a second twitch that rides on the "electrical coattails" of the first. This response is called summation.


Tetany, however, is a condition of physiological calcium imbalance. Manifests as tonic spasm of muscles; often associated with deficient parathyroid secretion.

Oxygen intake through mouth limited; unable to speak, swallow or consume solid foods due to laryngospasms; severity of spasms may cause mandible to fracture

The neurotransmitter involved in triggering skeletal muscle contractions is acetylcholine. Excitation-contraction coupling is the link (transduction) between the action potential generated in the sarcolemma and the start of a muscle contraction.

Severe tetanic muscle spasms can interfere with or stop breathing, invite pneumonia, cause cardiac arrest and/or brain damage from lack of oxygen. All of these may lead to death.

Complete recovery from a tetanus infection requires new nerve endings to grow, which can take up to several months. General symptoms will take awhile to abate

23-year-old male patient; has never received tetanus vaccination

Tattoo needle punctured deltoid muscle of shoulder repeatedly, introducing localized C. tetani to brachial region

Spastic paralysis of biceps and triceps; impaired ability to eat, use tools, drive and otherwise interact with environment, etc.

C. tetani bacterial spores introduced and spread to the central nervous system. Produces a toxin called tetanospasmin, blocking the nerve signals from patient's spinal cord to muscles.


This has lead to severe muscle spasms, rather than flaccid paralysis or tetany.

How Tetanus Impedes Chemically:


C. tetani interrupts the release of glycine and GABA, an inhibitory neurostransmitter that commands muscles to cease contraction. Without the release of glycine and GABA, excessive impulses rush through the nerves to the muscles, resulting in overstimulation of the muscles and excessive muscle contractions.

Kate Jones
BIOL 2401 (A&P I)
Case Map # 6 - NMJ