RESUMEN
OBJECTIVE: To describe a patient with a posterior inferior cerebellar artery stroke exhibiting a horizontal direction changing nystagmus with a complex clinical phenotype. MATERIALS AND METHODS: A 78-year-old man presented with acute vertigo and gait imbalance. He was dysphagic and ataxic on the left side. He had a fast, small-amplitude right-beating nystagmus in the primary gaze position and in the gaze towards the right. Towards the left, a coarse left-beating nystagmus was seen. RESULTS: Radiographic leftwards ocular deviation was evident on admission CT. Intravenous fibrinolysis was administered. 48-hour Holter-EKG, transthoracic ecochardiogram, and transcranial doppler were unremarkable. Brain MRI demonstrated an acute stroke involving the left medulla and cerebellum, mainly within the territory of the ipsilateral posterior inferior cerebellar artery. DISCUSSION AND CONCLUSIONS: Horizontal direction changing nystagmus can arise secondary to central lesions as brainstem strokes, it can be spontaneous or gaze-evoked and characteristically remains unchanged after fixation removal. In our case, the vestibular spontaneous and contralesional nystagmus was likely related to lower-brainstem damage; on the other hand, the ipsilesional gaze-evoked nystagmus might be related to lesions of the nucleus prepositus hypoglossi and/or cerebellum, both playing an important role in gaze-holding. Our findings suggest that central lesions with concurrent involvement of the ipsilateral vestibulo-ocular and horizontal gaze-holding pathways can cause direction changing nystagmus with complex phenotypes.
RESUMEN
Global neuropsychological impairments with intellectual disability (ID) seem to play a major role in the occurrence of psychogenic non-epileptic seizures (PNES) in epilepsy. Conversely, the pathophysiology underlying PNES combined with epilepsy without ID remains elusive. We investigated the neuropsychiatric profile in 26 average intelligent subjects (15 women, mean age: 40.04 ± 13.53 years) with temporal lobe epilepsy (TLE) plus PNES (TLE + PNES), compared with 28 with TLE and 22 with PNES alone, matched for age and sex. All subjects underwent neuropsychiatric assessment, including Beck Depression Inventory-2 (BDI-2), State-Trait Anxiety Inventory (STAI), Dissociative Experiences Scale (DES), Toronto Alexithymia Scale (TAS-20), Traumatic Experience Checklist (TEC), and cognitive evaluation. TLE + PNES and PNES groups shared a similar psychiatric profile with higher levels of depression (BDI-2, P < 0.001), anxiety (STAI-S, P < 0.001; STAI-T, P < 0.001), dissociation (DES, P < 0.001), and alexithymia (TAS, P = 0.005) scales than the TLE group. Nonetheless, like individuals with TLE, patients with TLE + PNES had a lower rate of a potentially traumatizing event than PNES. The very low rate of potentially traumatizing event in subjects with TLE + PNES leads us to hypothesize that epilepsy itself may be the psychophysiological distress that contributed to PNES. A psychopathological assessment in subjects with epilepsy is crucial to identify those more likely to develop PNES.