Case Presentation:

A 62‐year‐old right‐handed white man suddenly started crying at work without clear reason. En route to the emergency room (ER), he had multiple intermittent crying spells each lasted for about 5 minutes. On arrival, his blood pressure (BP) was 224/119, he was crying but responsive, and his consciousness was not impaired. There was no accompanying feeling of sadness. He denied headache, photophobia, blurred vision, difficulty swallowing, dysarthria, focal weakness, or numbness. Two hours after initiation of symptoms, the patient received 10 mg of intravenous labetalol in ER, his BP dropped to 182/95, and the crying spells stopped. The patient was afebrile, awake, and fully oriented; conventional psychological and extensive neurologic examinations (during and between the spells) were unremarkable. He had a history of uncontrolled hypertension, chronic obstructive lung disease, and heavy smoking; he denied alcohol, illicit drug abuse, or any recent change to his medications. Electrocardiogram, hemo‐gram, and basic chemistry were unremarkable. Brain computed tomography and magnetic resonance imaging showed hematoma in the lateral right basal ganglion 23 × 12 × 23 mm and mild local mass effect with 7‐mm surrounding vasogenic edema, but without midline shift. For 24 hours the patient remained asymptomatic; however, an interruption of antihypertensive medication administration (from interruption of intravenous access) caused his BP to gradually reach 220/110; then patient started crying for a few minutes, which completely resolved when his BP decreased to the 190s/90s range. No more crying spells were reported during his hospitalization.


Normal crying, a coordinated motor function involving facial and respiratory muscles, is triggered by specific stimuli, and accompanied by mood depression. Crying is termed pathological when the behavior is inappropriate or exaggerated and occurs without an apparent motivating stimulus. Pathological crying has been observed in patients with lesions involving diverse areas of the brain; however, the precise mechanism and neuroanatomy remains uncertain. Some postulated that the lesion occurs in the cerebroponto‐cerebellar pathways. It is known that limbic areas in the nondominant hemisphere are related more to the experiencing of negative emotions such as fear and anxiety than positive emotions such as happiness. Reported causes/presentations of pathological crying included pseudobulbar palsy, cerebrovascular event involving the pontine, capsular‐thalamic, or lenticularcaudate regions—“le fou rire pro‐dromique.” Some reported crying seizures episodes (diagnosed by an electroencephalogram during the spell) years after cerebral infarction.


To our knowledge there is no reported case of pathological crying as the only neurological manifestation of a basal ganglia bleeding event. It is important to note the association between very high blood pressure readings and the initiation of the crying spell, which is a unique characterization among pathological crying cases.


B. Obaid ‐ none; A. Sirelkhatim ‐ none