Phencyclidine (PCP) is a synthetic drug classified as a dissociative anesthetic, originally developed for use in human surgery but discontinued due to its severe side effects. It alters the perception of reality, leading to detachment, distorted senses, and confusion. A common physiological indicator of acute PCP intoxication is a noticeable change in pupil size, resulting from the drug’s complex interaction with the body’s involuntary control systems.
The Immediate Ocular Response to PCP
The direct answer is yes; PCP typically induces mydriasis, the medical term for pupillary dilation. This response is a frequently observed sign in patients presenting with acute PCP intoxication. The pupil expands, allowing more light to enter the retina.
The extent of dilation can vary significantly among individuals, depending on factors like the dose ingested, tolerance, and route of administration. Mydriasis is a common finding that helps clinicians quickly identify potential PCP exposure.
The Neurochemical Cause of Pupil Dilation
Pupil size is controlled by the autonomic nervous system, which operates through two opposing branches: the sympathetic and the parasympathetic systems. The sympathetic system, responsible for the “fight-or-flight” response, causes the iris dilator muscle to contract, opening the pupil (mydriasis). Conversely, the parasympathetic system manages “rest-and-digest” functions, causing the iris sphincter muscle to contract and constrict the pupil (miosis).
PCP acts as an indirect sympathomimetic agent, meaning it mimics the effects of the sympathetic nervous system. Its effect on pupil size stems from its action on monoamine neurotransmitters. Specifically, PCP inhibits the reuptake of norepinephrine and dopamine, increasing the concentration of these signaling molecules in the synaptic cleft.
The elevated levels of norepinephrine and dopamine stimulate adrenergic receptors associated with the sympathetic pathway, leading to increased activation of the iris dilator muscle. By boosting the activity of the sympathetic system, PCP overrides the parasympathetic tone, resulting in a widened pupil. This neurochemical cascade is the direct cause of the mydriasis observed during acute intoxication.
Other Visual Disturbances Associated with PCP
PCP intoxication is strongly associated with several other ocular symptoms that compromise vision. The most characteristic visual sign of PCP use is nystagmus, which involves rapid, involuntary movements of the eyes. This uncontrolled movement can present horizontally, vertically, or in a rotary pattern.
Nystagmus is a highly reliable indicator for clinicians, reported in a high percentage of intoxication cases. The involuntary eye movements occur because PCP affects the cerebellum, the brain region responsible for muscular coordination and balance. Users may also report blurred vision or double vision (diplopia), stemming from the drug’s disruption of the eye’s ability to focus.
Contextualizing the Acute Effects
Mydriasis and other visual changes are rarely isolated findings during a PCP-related episode. These ocular symptoms are part of a larger toxidrome, or constellation of signs, reflecting widespread stimulation of the central and autonomic nervous systems. The sympathomimetic effects that cause pupil dilation also trigger systemic responses such as elevated heart rate (tachycardia) and increased blood pressure (hypertension).
Other common physical manifestations include agitation, confusion, and sometimes bizarre or violent behavior. The combination of these effects, including muscle rigidity and decreased perception of pain, can lead to dangerously high body temperature (hyperthermia). The visual and systemic signs together provide a clinical picture recognized for identifying acute phencyclidine intoxication.