Weakness and facial droop: Is it a stroke?

CASE Sudden weakness

Ms. G, age 59, presents to a local critical access (rural) hospital after an episode of sudden-onset left-sided weakness followed by unconsciousness. She regained consciousness quickly and is awake when she arrives at the hospital. This event was not witnessed, although family members were nearby to call emergency personnel.

EXAMINATION Unremarkable

In the emergency department, Ms. G demonstrates left facial droop, left-sided weakness of her arm and leg, and aphasia. She says she has a severe headache that began after she regained consciousness. She is unable to see out of her left eye.

Ms. G’s NIH Stroke Scale score is 13, indicating a moderate stroke; an emergent head CT does not demonstrate any acute hemorrhagic process. Tissue plasminogen activator (tPA) is administered for a suspected stroke approximately 2 hours after her symptoms began. She is transferred to a larger, tertiary care hospital for further workup and observation.

Upon admission to the ICU, Ms. G’s laboratory values are: sodium, 137 mEq/L; potassium, 5.1 mEq/L; creatinine, 1.26 mg/dL; lipase, 126 U/L; and lactic acid, 9 mg/dL. The glucose level is within normal limits and her urinalysis is unremarkable.

Vital signs are stable and Ms. G is not in acute distress. A physical exam demonstrates 4/5 strength in the left-upper and -lower extremities. Additionally, there are 2+ deep tendon reflexes bilaterally in the biceps, triceps, and brachioradialis. She has left-sided facial droop while in the ICU, and continues to demonstrate some aphasia—although she is alert and oriented to person, time, and place.

The medical history is significant for depression, restless leg syndrome, tonic-clonic seizures, and previous stroke-like events. Medications include amitriptyline, 25 mg/d; citalopram, 20 mg/d; valproate, 1,200 mg/d; and ropinirole, 0.5 mg/d. Her mother has a history of stroke-like events, but her family history and social history are otherwise unremarkable.

The authors' observations

Conversion disorder requires the exclusion of medical causes that could explain the patient’s neurologic symptoms. It is prudent to rule out the most serious of the potential contributors to Ms. G’s condition—namely, an acute cerebrovascular accident. A CT scan did not find any significant pathology, however. In the ICU, an MRI showed no evidence of acute infarction based on diffusion-weighted imaging. A head and neck MRA demonstrated no hemodynamically significant stenosis of the internal carotid arteries. An EEG revealed generalized, polymorphic slow activity without evidence of seizures or epilepsy. An electrocardiogram showed normal ventricular size with an appropriate ejection fraction.

The ICU staff consulted psychiatry to evaluate a psychiatric cause of Ms. G’s symptoms.

An exhaustive and comprehensive workup was performed; there were no significant findings. Although laboratory tests were performed, it was the physical exam that suggested the diagnosis of conversion disorder. In that sense, the diagnostic tests were more of a supportive adjunct to the findings of the physical examination, which consistently failed to indicate a neurologic insult.

Hoover’s sign is a well-established test of functional weakness, in which the patient extends his (her) hip when the contralateral hip is flexed. However, there are other tests of functional weakness that can be useful when considering a conversion disorder diagnosis, including co-contraction, the so-called arm-drop sign, and the sternocleidomastoid test. Diukova and colleagues reported that 80% of patients with functional weakness demonstrated ipsilateral sternocleidomastoid weakness, compared with 11% with vascular hemiparesis.¹

Ms. G appeared to have suffered an acute ischemic event that caused her neurologic symptoms; her rather extensive psychiatric history was overlooked before the psychiatric service was consulted. When Ms. G was admitted to the ICU, the working differential was postictal seizure state rather than cerebrovascular accident. Ms. G had a poorly defined seizure history, and her history of stroke-like events was murky, at best. She had not been treated previously with tPA, and in all past instances her symptoms resolved spontaneously.

Ms. G’s case illustrates why conversion disorder is difficult to diagnose and why, perhaps, it is even a dangerous diagnostic consideration. Booij and colleagues described two patients with neurologic sequelae thought to be the result of conversion disorder; subsequent imaging demonstrated a posterior stroke.² Over a 6-year period in an emergency department, Glick and coworkers identified six patients with neurologic pathology who were misdiagnosed with conversion disorder.³ In a study of 4,220 patients presenting to a psychiatric emergency service, three patients complained of extremity paralysis or pain, which was attributed to conversion disorder but later attributed to an organic disease.⁴