66-year-old right-handed female who presented after acute-onset behavioral changes starting five days prior. Although anosognosic to these changes, family endorsed sudden onset personality changes accompanied by insomnia, headache, and disinhibition in the form of profuse logorrhea. No focal neurological symptoms were reported at onset or following the episode. After a psychiatric evaluation revealed no psychiatric pathology to which the symptoms could be attributed, neurological consultation was recommended to assess for an organic etiology.

Mental status examination showed an alert and oriented female that demonstrated intact language and memory faculties, albeit being profusely logorrheic and circumstantial in her speech patterns. Her neurological examination was normal. CT Head without contrast demonstrated an incidental 1.3 cm right thalamic hemorrhage. MRI of the brain confirmed right thalamic hemorrhage, in addition to mild surrounding vasogenic edema extending to the right cerebral peduncle; no microhemorrhages were noted on gradient-echo or susceptibility weighted images (cortical or otherwise). MR Angiogram did not show any vascular abnormalities. MR Perfusion did not show any hemodynamic changes. 

Despite hemorrhagic strokes of the thalamus secondary to chronic hypertension being a common entity, purely behavioral manifestations as their sole symptomatic expression are relatively uncommon. The thalamus is schematically understood as the nervous system’s relay center mediating functions from the sensorimotor to the cognitive-behavioral. Numerous pathways exist in a multitude of orientations, from unidirectional to reciprocal and from diffuse to specific, providing orderly chaos to neurological input-output circuits. Amongst its nuclei, the medio-dorsal nuclei of the thalamus seem to be most intimately interconnected with the prefrontal cortices via thalamocortical connections that radiate to the ventrolateral prefrontal cortices, the dorsolateral prefrontal cortices and, most relevant to this discussion, the orbitofrontal cortices. This suggests a possible deep brain substrate for a frontal-like disinhibition syndrome in the absence of cortical or fascicular damage.