Case Studies in Toxicology: An Unlikely Cause of Paralysis
Case
An Asian man in his third decade, with a medical history of hypertension and hyperlipidemia, and who had recently been involved in a motor vehicle collision (MVC), presented to the ED with a chief complaint of severe bilateral upper and lower extremity weakness. The patient noted that the weakness had begun the previous evening and became progressively worse throughout the night, to the point that he was unable to move any of his extremities on the morning of presentation.
Upon arrival at the ED, the patient was awake, alert, and oriented to self, time, and place; he also spoke in full sentences without distress. He denied fever, chills, difficulty breathing, or preceding viral illness. The patient stated that he was not taking any medications and denied a history of alcohol, tobacco, or drug abuse.
Initial vital signs at presentation were: blood pressure, 141/50 mm Hg; heart rate, 90 beats/min; respiratory rate, 16 breaths/min; and temperature, 97.4°F. Oxygen saturation was 100% on room air. On physical examination, the patient was in no acute distress and had a normal mental status. His pupils were normally reactive and his other cranial nerves were normal. Muscle strength in the upper and lower extremities was 1/5 with 1+ reflexes bilaterally, and there was no sensory deficit. The patient was placed on continuous cardiac monitoring with pulse oximetry.
What is the differential diagnosis for acute extremity weakness or paralysis?
The differential diagnosis for acute symmetrical extremity weakness or paralysis is broad and includes conditions of neurological, inflammatory, and toxic/metabolic etiologies.1 Neurological diagnoses to consider include acute stroke, specifically of the anterior cerebral or middle cerebral artery territories; Guillain-Barré syndrome; myasthenia gravis; spinal cord compression; and tick paralysis. Acute ischemic or hemorrhagic stroke most frequently presents with unilateral upper or lower extremity weakness accompanied by garbled speech and sensory deficits. Patients who have suffered a brainstem or cerebellar stroke commonly present with alterations of consciousness, visual changes, and ataxia. Posterior circulation strokes are also characterized by crossed neurological deficits, such as motor deficits on one side of the body and sensory deficits on the other.
Spinal Cord Pathology. Signs and symptoms of spinal cord compression or inflammation vary widely depending on the level affected. Motor and sensory findings of spinal cord pathology include muscle weakness, spasticity, hyper- or hyporeflexia, and a discrete level below which sensation is absent or reduced.
Guillain-Barré Syndrome. Patients who have Guillain-Barré syndrome (a disease of the myelin sheaths of the peripheral nerves) often present with complaints of numbness or paresthesias in the extremities.2 The condition is characterized by progressive symmetric muscle weakness accompanied by absent or depressed deep tendon reflexes and is typically associated with a recent exposure to an infectious agent such as a viral upper respiratory infection, bacterial infection, or vaccine.
Myasthenia Gravis. Myasthenia gravis is a disease of the neuromuscular junction. It presents with weakness in any muscle group, and the muscles are easily fatigued by repetitive use.
Toxic Exposures. Toxins, such as botulinum, ixovotoxin, nicotine, succinylcholine, and tetrodotoxin, are prominent, though less common, causes of muscular weakness or paralysis. Botulinum toxin acts at the neuromuscular junction. Patients with botulism typically present with a gastrointestinal prodrome of nausea, vomiting, and diarrhea followed by cranial nerve dysfunction and descending muscle weakness.3
Tetrodotoxin, nicotine, and curare-like paralytics act at the motor end plate of the neuromuscular junction to produce neuromuscular blockade with subsequent muscular weakness or paralysis. Similarly, ixovotoxin, the toxin responsible for tick paralysis, causes ascending flaccid paralysis by decreasing the release of acetylcholine at the neuromuscular junction.3
Metabolic and Endocrine Disorders. Conditions such as hypokalemia, hypomagnesemia, and periodic paralysis can also present with neurological complaints such as generalized weakness and paresthesias. Of note, it is important to differentiate true neuromuscular weakness from weakness secondary to limited effort.
Case Continuation
Because of the patient’s history of an MVC, cervical cord compression was considered concerning enough to require exclusion through magnetic resonance imaging (MRI) of the cervical spine. However, upon arrival at the MRI suite, the patient became severely tachypneic and tachycardic, and was unable to tolerate lying flat. He was intubated for impending respiratory failure. Laboratory results from blood drawn prior to transport to MRI were reported immediately after the resuscitation and were notable for the following: potassium, <1.5 mEq/L; bicarbonate, 20 mEq/L; creatine kinase, 889 U/L; ethanol, not detected.
