A 56-year-old man with a dominant right hand presented to a local hospital emergency department because he was having difficulty walking. He received a tapering dose of prednisone, which slightly improved his symptoms. However, within 2 days, his symptoms worsened again.
Two weeks later, the patient presented to a neurology office with complaints that he could not ambulate for 2 weeks. On relating his medical history to a neurologist (C.H.), the patient reported that approximately 20 years ago, he had an episode of weakness in his left leg. He had presented to his primary care physician, who diagnosed MS. The physician prescribed medication (unknown by the patient), and the patient's symptoms improved. The patient was on the medication for what he described as a “short time.” No further diagnostic intervention or treatment had been provided.
In addition to the patient's history of MS, he had hypercholesterolemia and hypothyroidism, for which he was taking simvastatin (20 mg) and levothyroxine sodium (112 μg), respectively. He had no known drug allergies.
On physical examination, the patient's blood pressure was 132/60 mm Hg; heart rate, 100 beats per minute; and weight, 142 lbs. The patient was pleasant and cooperative, and he followed commands and answered questions appropriately. However, while he was describing a recent fall that occurred while walking his dog, the patient broke into an uncontrollable laughter. He laughed so hard that his eyes began to tear, and he could not stop laughing for several minutes. Several such laughing fits occurred throughout the visit without any apparent stimulus. His wife remarked that “he was never like this before.”
On examination of the cranial nerve, the patient had no afferent pupillary defect (Marcus Gunn pupil), internuclear ophthalmoplegia, nystagmus, or facial asymmetry. Extraocular eye movements were intact. He had a good shoulder shrug. The patient had normal motor skills, good muscle bulk and tone, and strength in all four extremities. The rest of the neurologic examination revealed that the patient had difficulty with ambulation because of ataxia, which caused him to lean to one side and resulted in a tandem gait. He had impaired vibratory sensation in his feet, and his joint position sense was slightly impaired in his toes. Results from an electroencephalography were normal and without evidence of gelastic epilepsy.
The patient received 500 mg/d of intravenous prednisone as an outpatient for 4 days. His episodes of pathological laughter decreased in frequency but did not resolve completely. Selective serotonin reuptake inhibitors were discussed as a treatment option for the patient's periodic episodes of pathological laughter, but the patient declined further treatment.
Follow-up magnetic resonance imaging taken 6 weeks after presentation revealed periventricular white matter lesions and “Dawson fingers” (Figure), which are consistent with MS.