A Lesion Approach to Neurobiology of Dissociative Symptoms

A 71-year-old woman with history of hypertension, type 2 diabetes mellitus, and two prior episodes of transient ischemic attacks, presented to the emergency department with an episode of “getting disoriented.” While driving, the patient suddenly felt that the route seemed unfamiliar, and she inadvertently took a wrong exit, which was brought to her attention by her companions. Meanwhile, she also felt that something was wrong with her own person, as her mind went blank and she felt as is she was in a daze. The whole episode lasted half an hour. In the emergency department, the patient recalled that the trees around the route looked “different” and that everything was happening effortlessly with her being a passive spectator. She denied any changes in perception of color, sound, and recognition of faces and had no neglect symptoms. Her neurological examination was unremarkable except for left inferior quadrantanopia. Magnetic resonance imaging of the brain showed new infarcts in the right occipital cortex, right thalamus, and head of right caudate. The patient had an uneventful hospital stay without recurrence of these symptoms.

The patient's symptoms are redolent of derealization and depersonalization. Although lesions of the occipital cortex have been reported in patients with dissociative symptoms, only rarely has involvement of thalamus been reported.¹ Thalamic hypofunction has been shown in disorders associated with dissociative symptoms such as posttraumatic stress disorder (PTSD).² While the involvement of the visual cortex with the resultant visuo-limbic disconnection may in part explain the symptoms of derealization,³ thalamic dysfunction may contribute to depersonalization by interfering with the initial processing of perceptual information about the “self.” This hypothesis is explored below.

The parietal lobe is one of the regions involved in generating the body schema,⁴ and the thalamo-cortico-thalamic loop is implicated in “conscious awareness” in the perceptual domain.⁵ The corticothalamic synapses (including those from the parietal lobe) on the relay nuclei of the bilateral thalami are excitatory and enhance the transmission of peripheral information toward the cortex. The output of the thalamus, however, is to the cortex of the same side.⁶ Thus, with the infarction of right thalamus, as in this patient, one speculates a possible corticopetal disconnection between the right thalamus and the right parietal lobe, which in turn reduces the feedback cortical enhancement of the thalami. This may result in a compensatory overactivity in the parietal lobes, thus interfering with the flow of “relevant” information into the thalami and impairing their sensory gating function.⁵ The overactivity in the parietal region is supported by a recent positron emission tomography study that showed increased activity in the parietal somatosensory association area in patients with depersonalization disorder.⁴ Hence, as highlighted by some investigators,³ depersonalization and derealization may have separate neuroanatomical correlates, which needs further exploration. Interestingly, glutamate, which is known to increase after stroke and environmental stress, is speculated to cause dissociative symptoms in PTSD,⁷ a notion favored by this report.