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The toxin acts after incubation period (3-14) days) at several sites within central nervous system, including peripheral motor end plates, spinal cord, brain and sympathetic nervous system. The typical clinical manifestations of tetanus are caused when tetanus toxin interferes with release of neurotrasmitters, blocking inhibitor impulses.

Blockade of spinal inhibition is produced when toxin acts at synapse of interneurons of inhibitory pathways and motor neurons. General muscle rigidity arises from uninhibited afferent stimuli entering central nervous system from periphery. The effect of toxin on brain is controversial; direct inoculation can cause seizures.

One of many complications from tetanus is respiratory failure secondary to spasms, obstruction by secretions, exhaustion and pulmonary aspiration. Cardiovascular complications thought to be due to hyperactivity of sympathetic nervous system include tachycardia, with heart rates over 180 beats per minute, severe vasoconstriction and hypertension. Autonomic dysfunction is seen as increased basal sympathetic activity and episodes of sympathetic over activity. (SOA).