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J Neurol Neurosurg Psychiatry 67:255 doi:10.1136/jnnp.67.2.255
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Crying spells as symptoms of a transient ischaemic attack

  1. MARIO F MENDEZ,
  2. YURI L BRONSTEIN
  1. Department of Neurology, University of California at Los Angeles, West Los Angeles Veterans Affairs Medical Center, Los Angeles, CA, USA
  1. Dr MF Mendez, Neurobehavior Unit (691/116AF), West Los Angeles V.A. Medical Center, 11301 Wilshire Blvd, Los Angeles, CA 90073, USA. Telephone 001 310 478 3711 ext 42696; fax 001 310 268 4181; email mmendez{at}UCLA.edu

    In the absence of depression, crying spells associated with neurological disease usually result from pseudobulbar palsy or, more rarely, from crying seizures. To our knowledge, there are no prior reports of crying spells heralding or signifying a transient ischaemic attack. We report on a patient with prominent cerebrovascular risk factors who had a transient episode of intractable crying and focal neurological findings.

    The patient was a 55 year old right handed man who presented with acute, uncontrolled crying spells followed by left sided paraesthesias. Around 6 00 am he awoke with a diffuse, pressure headache and suddenly started crying for no apparent reason. There was no accompanying feeling of sadness. This crying, which involved lacrimation and “sobbing,” abruptly ceased after 5 minutes. Within 30 minutes of his initial crying spell, his headache had resolved but he became aware of numbness over his left face and numbness and pain in his left neck and arm. The numbness was not progressive, and the patient did not complain of paraesthesias in his trunk or left leg. He denied photophobia, nausea or vomiting, blurred vision, visual obscurations, difficulty swallowing, dysarthria, or focal weakness. Over the next 2 to 3 hours, he had five more crying spells, each lasting 5 to 10 minutes, occurring out of context, without precipitating factors or sadness, with an acute onset and offset, and without alteration of consciousness. The patient’s left face and arm numbness persisted during and between these crying spells but abruptly resolved shortly after his last crying spell. This patient had hypertension, diabetes mellitus, coronary artery disease, an old myocardial infarction, raised cholesterol concentrations, and a history of heavy smoking.

    On examination between recurrent crying spells, his blood pressure was 143/92 with a regular pulse of 62, and there were no carotid bruits. His mental status was normal. Cranial nerve examination disclosed a flattening of the left nasolabial fold and decreased pinprick sensation over his left face with an occasional mild facial twitching. Cranial nerves IX-XII were intact, and gag reflex and palate elevation were normal. He did not have dysarthria or a brisk jaw jerk. The rest of the neurological examination showed mild weakness in his left upper arm, and decreased pinprick and temperature sensation over the left half of his body. His reflexes were +2 and symmetric with downgoing toes.

    The patient lacked prior depression, new depressive symptoms, or prior crying spells as an adult except for a single episode during dental anaesthesia. At the time of his admission, he had not had any recent adverse events in his life, and was totally surprised by his reaction.

    The patient’s crying spells, paraesthesias, and neurological findings entirely resolved within about 3 hours. Routine laboratory tests, ECG, and CT were normal. Two days after admission, MRI disclosed a mild degree of white matter capping over the right frontal horn, and an EEG showed frontal intermittent rhythmic delta activity but no epileptiform changes. Carotid Doppler studies showed atherosclerotic changes without haemodynamically relevant obstruction. He was discharged on antiplatelet therapy with aspirin.

    These results suggest that crying spells can be a manifestation of a transient ischaemic attack. He presented with paroxysmal crying spells followed by a left sided hypaesthesia and a mild left sided weakness, all of which resolved. His crying was non-emotional, inappropriate to the context, and did not correspond to his underlying mood. Moreover, the patient had multiple vascular risk factors supportive of a cerebrovascular aetiology for his episode.

    The most common cause of pathological crying is pseudobulbar palsy, a complication of strokes and other diffuse or bihemispheric brain damage.1 Pseudobulbar palsy results from bilateral interruption of upper motor neuron innervation of bulbar motor nuclei and brainstem centres. In addition to crying, pseudobulbar palsy may include dysarthria, dysphagia, bifacial weakness, increased facial and mandibular reflexes, and weak tongue movements. There were no signs or symptoms of pseudobulbar palsy in this patient.

    Crying or dacrystic seizures also occur but are rare. These seizures are part of the range of complex partial seizures and usually emanate from the right temporolimbic system.2 Crying seizures may result from prior cerebral infarctions.3 Although our patient had mild twitching of his left face, he did not have other evidence suggesting definite seizure activity.

    It is likely that this patient had a single transient ischaemic attack with multiple crying spells. The localisation of his attack is unclear; involvement of the right thalamus or neighbouring internal capsule is a possibility. Similar to spells of laughter, spells of crying may occur in relation to unilateral cerebrovascular events. Although most reports of crying after unilateral strokes have reported left hemispheric lesions,4 crying also may result from right hemispheric strokes.4 Even more similar to our patient, sudden laughing spells, “le fou rire prodromique,” rarely precede strokes involving the left capsular-thalamic, lenticular-caudate, or pontine regions.5 Our patient may have had a comparable phenomenon from the right hemisphere. The mechanism for this phenomenon may have been temporary activation or stimulation of ischaemic motor pathways.

    References

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