LAUSR

A small punctuate lesion in the hippocampus can cause acute amnesia, confabulation, and altered consciousness, and it represents a typical radiologic finding of transient global amnesia (TGA). Herein, we report our experiences on six patients with hippocampal lesions presenting with acute vestibular syndrome (AVS). Two years earlier, a 63-year-old man with diabetes mellitus presented with acute vertigo for 2 days. The patient denied headache, diplopia, tinnitus, ear fullness, or hearing loss. At presentation, the patient was alert, attentive, and oriented. Examination showed left-beating spontaneous nystagmus without visual fixation (Fig. 1A), which increased after horizontal head shaking. Video head-impulse tests (HITs) were pathological for right horizontal canal (HC, Fig. 1B). Bithermal caloric tests showed right canal paresis of 44%. Sinusoidal harmonic acceleration documented phase leads of the vestibulo-ocular reflex (VOR) in the presence of normal gains and symmetry. DWI revealed a discrete lesion in the right hippocampal tail (Fig. 1C, Patient 1). Transcranial Doppler with saline contrast, echocardiogram, and Holter monitoring were negative for embolic sources. The vertigo improved over the following 2 weeks with resolution of the spontaneous nystagmus. Six months later, however, the patient experienced recurrence of the vertigo as well as re-emergence of the left-beating spontaneous nystagmus and abnormal HITs for the right HC (Table 1, patient 1). A punctuate lesion was not visible on follow-up DWI at then. Since then, we came across five more patients presenting with AVS in association with punctuate hippocampal lesions on diffusion-weighted images (DWIs, Table 1, Fig. 1C). Three of them showed bilateral lesions. The presenting symptoms included vertigo (n = 4), retrograde and anterograde amnesia (n = 3), and headache (n = 3) disequilibrium (n = 2), and nausea/vomiting (n = 2). HITs were abnormal in four patients, for the HC in four and for the posterior canal in one. Bithermal caloric tests showed a canal paresis in five patients, to the left in two patients with bilateral MRI lesions, and to the lesion side in the remaining three with a unilateral lesion (Table 1). None of the patients had any previous history of dizziness or headache that may explain the vestibular impairments. Besides, all of our patients showed negative results for an embolic source. Patients’ vertigo resolved completely (n = 4) or improved markedly (n = 2) within 2 weeks. Over a 1-year-follow-up period, AVS recurred in one patient (1/6, 17%, patient 1). Meanwhile, follow-up evaluation showed disappearance of the spontaneous nystagmus (5/6, 83%) along with normalization of the HITs (2/3, 67%) and canal paresis (1/4, 25%, Table 1). Prior reports regarding clinical and radiological aspects of punctuate hippocampal lesion are scarce, but they are regularly found in patients with TGA. However, apart from its role for memory and emotion processing, the hippocampus also plays critical role for relaying ascending vestibular signals. Accordingly, 40% of patients having a punctuate lesion in this area reported vertigo and dizziness in an MRIbased patient series [1]. The relationship between hippocampal lesions and vestibular dysfunction remains to be delineated in our patients. Dizziness and nausea/vomiting can accompany hippocampal lesions [1], and may occur during the acute stage of TGA [2]. Similarly, cerebral lesions can also present with spontaneous or positional nystagmus especially * Sun‐Uk Lee [email protected]