I would like to comment on both the temporal and neuroanatomical aspects of the case of crying spells as symptoms of a transient ischaemic attack (TIA), presumed to involve the right capsular-thalamic region, recently reported by Mendez and Bronstein.1

As the authors point out, laughter preceding a cerebrovascular event involving the pontine, capsular-thalamic, or lenticular-caudate regions (“le fou rire prodromique”) is a rare but well recognised phenomenon, first described almost a century ago. However, they do not mention previous reports of pathological crying heralding ischaemic vascular events,2-4 including one patient with TIA.3 The term “les folles larmes prodromiques” has been suggested for this phenomenon.4 In the series of Davison and Kelman,2 case 36 was a hypertensive female patient who had two cerebrovascular events 3 years apart, in the second of which the “ictus was associated with frequent spontaneous crying spells”; there were left sided pyramidal signs, and a right capsular-thalamic insult was suspected.2 Tatemichiet al 3 reported seven patients with basilar ischaemia, in one of whom involuntary weeping was the first symptom; another patient had TIAs with subclavian steal in whom “explosive crying” was a conspicuous feature, along with diplopia, dysarthria, and gait instability. A more recent report presented a case of embolic occlusion of the top of the basilar artery heralded by pathological crying, with probable bilateral midbrain infarction (interpretation was complicated by acute intra-arterial thrombolytic therapy).4

As with laughter, the neuroanatomical substrates of crying are diffuse. Both are reflexive pontomedullary activities controlled by at least two supranuclear pathways: a volitional pathway running in the corticobulbar pathways of the posterior limb of the internal capsule; and a more anterior pathway, presumably with inputs from the limbic system, running rostral to the knee of the internal capsule carrying inhibitory and/or facilitatory fibres.5 The correlation of pathological crying occurring after strokes with damage to brain areas involved in serotoninergic neurotransmission,6 and the response of such crying to specific serotonin reuptake inhibitors,7 suggests the involvement of the brainstem raphe nuclei and their projections in the pathogenesis of pathological crying. As demonstrated by these cases,1-4 both transient and focal brain insults, as well as chronic and diffuse brain disease, may cause crying spells, presumably by interrupting descending inhibitory input to a brainstem “crying centre”.