The hippocampus is a small but complex anatomical structure that plays an important role in spatial and episodic memory. The hippocampus can be affected by a wide range of congenital variants and degenerative, inflammatory, vascular, tumoral and toxic-metabolic pathologies. Magnetic resonance imaging is the preferred imaging technique for evaluating the hippocampus. The main indications requiring tailored imaging sequences of the hippocampus are medically refractory epilepsy and dementia. The purpose of this pictorial review is threefold: (1) to review the normal anatomy of the hippocampus on MRI; (2) to discuss the optimal imaging strategy for the evaluation of the hippocampus; and (3) to present a pictorial overview of the most common anatomic variants and pathologic conditions affecting the hippocampus.Teaching points • Knowledge of normal hippocampal anatomy helps recognize anatomic variants and hippocampal pathology. • Refractory epilepsy and dementia are the main indications requiring dedicated hippocampal imaging. • Pathologic conditions centered in and around the hippocampus often have similar imaging features. • Clinical information is often necessary to come to a correct diagnosis or an apt differential.

Hypertrophic olivary degeneration (HOD) is a unique form of transneuronal degeneration caused by a disruption of the dentato-rubro-olivary pathway, also known as the triangle of Guillain-Mollaret. The triangle of Guillain-Mollaret is involved in fine voluntary motor control and consists of both the inferior olivary nucleus and the red nucleus on one side and the contralateral dentate nucleus. Clinically, patients classically present with symptomatic palatal myoclonus. Typical magnetic resonance imaging findings include T2-hyperintensity and enlargement of the inferior olivary nucleus evolving over time to atrophy with residual T2-hyperintensity. In this article, we provide a case-based illustration of the anatomy of the Guillain-Mollaret-triangle and the typical imaging findings of hypertrophic olivary degeneration.

Absence of the PPBS can be seen in 4.1% of patients undergoing MRI of the brain for non-endocrinological reasons. Neither field-strength nor the use of a thick-sliced 2D T1-SE versus a thin-sliced 3D T1-GE sequence influenced the detectability of the PPBS. There is a statistically significant association between increasing age and male sex and the absence of the PPBS.

A 69-year-old male was admitted to the emergency department with suspicion of a recurrent cerebrovascular accident (CVA). Medical history included a prior CVA in the vascular supply area of the left middle cerebral artery in 2010, due to a patent foramen ovale, causing cardiogenic emboli (Fig. A). The patient was respectively treated with anticoagulation and percutaneous closure of the foramen; a significant motoric aphasia persisted. At a neurologic clinical investigation, besides the known aphasia, apraxia of the tongue, dysarthria and a limited left hemisyndrome were noted with predominant paresis of the left hand and impairment of the left visual field. Imaging was requested, with CT only showing age-related atrophic changes and sequelae of left middle cerebral artery infarction. MRI revealed additional diffusion restriction in the right opercular region, suggestive of recent stroke (Fig. B).Holter monitoring revealed paroxysmal atrial flutter, confirming the suspicion of cerebral infarction as the basis of cardiogenic emboli. Following the recent ischaemia, the speech-language pathologist noticed the patient was not able to eat, but when food was deposited in his mouth, no eating difficulties or swallowing impairment were observed. Patient was treated with anticoagulant regimen, percutaneous entero-gastrostomy, anti-epileptic drugs and neurologic revalidation. CommentFacio-labio-pharyngo-glosso-masticator paralysis, also known as Foix-ChavanyMarie or opercular syndrome, consists of dissociation between automatic and voluntary movements. Bilateral lesions in the operculum cause a loss of volitional control of lingual, pharyngeal, facial and masticatory musculature, with preserved automatic movement. Typical manifestations include difficulties in mouth opening, tongue protrusion, chewing and swallowing food as well as speech impairments. Opercular syndrome may be congenital or acquired (as is the case in our patient), and intermittent or persistent. Possible causes of opercular syndrome include cerebrovascular disease (acute setting), CNS infections (subacute form), neuronal migration disorders (developmental), neurodegenerative disorders or epilepsy (reversible). Most reported cases, like our case, can be attributed to thrombo-embolism of middle cerebral artery branches, which irrigate the operculum.The operculum represents the cortex surrounding the insula, and can be divided into three parts: the frontal operculum, the frontoparietal operculum and the temporal operculum; with variable involvement of the subcortical white matter. Bilateral lesions in these areas clinically mimic a pseudobulbar palsy in the distribution of the 5 th , 7 th , 9 th , 10 th and 12 th cranial nerves. The so-called "automatic-voluntary dissociation" can be elucidated by analysis of functional neuro-anatomy. Volitional control of the facial, oral and pharyngeal musculature demands intact motor cortices and pyramidal pathways; pathology in these areas leads to a selective palsy of voluntary use of these muscle groups. Emotional or s...