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Lance–Adams syndrome (LAS) is a sequela of hypoxic encephalopathy due to respiratory arrest, airway obstruction, cardiac arrest, etc., several days after the onset of hypoxic encephalopathy. A condition that presents with functional myoclonus associated with increased cortical excitability in a few weeks.
Action myoclonus is the most disabling form of myoclonus and can affect the arms, legs, face, and even the voice. It is often associated with tonic-clonic seizures and diffuse neuronal disease such as post-hypoxic encephalopathy , uremia , and the various forms of PME, although, in the case of focal cerebral damage, the disease may be ...
Familial adult myoclonus Epilepsy (FAME) This is a condition characterized by the repetition of non-coding sequences and has been identified using various abbreviations. Initially, it was associated with four primary gene locations: FAME1 (8q23.3–q24.1), FAME2 (2p11.1–q12.1), FAME3 (5p15.31–p15.1), and FAME4 (3q26.32–3q28).
Symptoms often include action or stimuli induced myoclonus, seizures, neuropathy, cognitive decline, and spike and wave or no cerebral discharges. [4] The prognosis of those diagnosed with PME is poor. The person often becomes reliant on a wheelchair, enters a vegetative state due to myoclonus, and has a shortened life expectancy. [4] [3]
Myoclonic astatic seizures: seizures that involve a myoclonic seizure followed immediately by an atonic seizure. This type of seizure is exclusive to MAE and is one of the defining characteristics of this syndrome. Tonic seizures: muscle stiffening or rigidity. This seizure is rare in this syndrome.
A paper published in 2023 showed that burst suppression and epilepsy may share the same ephaptic coupling mechanism. [6] When inhibitory control is sufficiently low, as in the case of certain general anesthetics such as sevoflurane (due to a decrease in the firing of interneurons [7]), electric fields are able to recruit neighboring cells to fire synchronously, in a burst suppression pattern.
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The primary diagnosis for JME is a good knowledge of patient history and the neurologist's familiarity with the myoclonic jerks, which are the hallmark of the syndrome. [38] Additionally, an EEG will indicate a characteristic pattern of waves and spikes associated with the syndrome such as generalized 4–6 Hz polyspike and slow wave discharges.