Epilepsy and Alzheimer’s disease (AD) incidence increases with age. There are reciprocal relationships between epilepsy and AD. Epilepsy is a risk factor for AD and, in turn, AD is an independent risk factor for developing epilepsy in old age, and abnormal AD biomarkers in PET and/or CSF are frequently found in late-onset epilepsies of unknown etiology. Accordingly, epilepsy and AD share pathophysiological processes, including neuronal hyperexcitability and an early excitatory–inhibitory dysregulation, leading to dysfunction in the inhibitory GABAergic and excitatory glutamatergic systems. Moreover, both β-amyloid and tau protein aggregates, the anatomopathological hallmarks of AD, have proepileptic effects. Finally, these aggregates have been found in the resection material of refractory temporal lobe epilepsies, suggesting that epilepsy leads to amyloid and tau aggregates. Some epileptic syndromes, such as medial temporal lobe epilepsy, share structural and functional neuroimaging findings with AD, leading to overlapping symptomatology, such as episodic memory deficits and toxic synergistic effects. In this respect, the existence of epileptiform activity and electroclinical seizures in AD appears to accelerate the progression of cognitive decline, and the presence of cognitive decline is much more prevalent in epileptic patients than in elderly patients without epilepsy. Notwithstanding their clinical significance, the diagnosis of clinical seizures in AD is a challenge. Most are focal and manifest with an altered level of consciousness without motor symptoms, and are often interpreted as cognitive fluctuations. Finally, despite the frequent association of epilepsy and AD dementia, there is a lack of clinical trials to guide the use of antiseizure medications (ASMs). There is also a potential role for ASMs to be used as disease-modifying drugs in AD.

BackgroundBackground: Magnesium is an important intracellular cation involved in essential enzymatic reactions. It is necessary for neuronal function and its depletion can produce neurological symptoms such as cramps or seizures. Clinical consequences of its deficit in the cerebellum are less known and the diagnosis can be delayed because of the lack of awareness on this condition. Cases Cases: We present three cases of cerebellar syndrome (CS) due to hypomagnesemia: A midline CS with myoclonus and ocular flutter and two cases of hemispheric CS, one of them entailed a Schmahmann's syndrome and the other suffered a seizure. MRI findings revealed cerebellar vasogenic edema and the symptoms improved after magnesium replacement in all cases. Literature Review Literature Review: We reviewed 22 cases of CS due to hypomagnesemia, all with subacute onset (days to weeks). Encephalopathy and/or epileptic seizures were common. MRI findings were vasogenic edema involving the cerebellar hemispheres, the vermis, or the nodule. Up to 50% of patients presented hypocalcemia and/or hypokalemia. All the patients showed symptomatic improvement after magnesium replacement, but 50% showed significant sequelae, and 46% relapsed. Conclusions Conclusions: Hypomagnesaemia should always be considered in the differential diagnosis of CS as it has a potential treatment, and its early recognition can avoid recurrences and permanent cerebellar impairment.

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