- Messages
- 2,397
- Reaction score
- 10
- Points
- 0
Howdy
Here's something I found
Precipitating Stimuli for Reflex Seizures
Here's something I found
Seizures induced by eating
Seizures induced by eating are characterized by seizures closely related to one or several parts of eating. The clinical triggers of a seizure are usually stereotyped for each patient, but patients may have some points in common. Rare patients have seizures at the very sight or smell of food; others may have them immediately after a heavy meal suggesting gastric distension as a trigger in such cases (Gastaut and Poirier, 1964). Seizures with eating are typically focal motor seizures, with or without auras or automatisms of temporolimbic type, almost always related to a symptomatic epilepsy. Seizures induced by eating are usually associated with localized or regional EEG epileptiform activity either from temporolimbic structures or from suprasylvian regions in association with larger lesions. EEG epileptiform activity that is generalized from the start is rare.
Rémillard and associates suggested that patients with temporolimbic seizures activated by eating have fewer spontaneous attacks and are more likely to have such attacks from the onset of their epilepsy than are patients with extralimbic, usually suprasylvian, seizure onset who have less constant activation by eating. Patients with suprasylvian seizure onset usually have more obvious extratemporal structural lesions and possible activation by specific thalamocortical afferents (Rémillard et al 1998). They may also have seizures with other forms of buccal stimulation such as tooth brushing or kissing. Koutroumanidis et al (2001) reported a case of adult-onset sensitivity to toohbrushing only, with normal imaging and interictal left frontal epileptiform activity and suggested that this was a cryptogenic reflex epilepsy.
Many patients with eating epilepsy have seizures that can be activated only by obvious combinations of stimuli (Fiol et al 1986), and alerting stimuli have been reported to abolish attacks (Ganga et al 1988), providing at least circumstantial evidence for involvement of an increasing cortical mass and of subcortical influences, which may promote or inhibit seizure occurrence in some cases of reflex epilepsy. It appears that localization of seizure onset and the nature of the seizure trigger are related in these attacks. Patients with suprasylvian lesions may be triggered by other oral activities and may represent a particularly noticeable type of seizure induced by proprioceptive or by somatosensory stimulation. They may be different from patients with temporolimbic-onset seizures, in whom taste and autonomic afferents may play a more important role, and in some of whom seizures may also be related to emotional or autonomic components of eating or to gastric distension, with possible participation of limbic and autonomic afferents.
A prevalence of approximately 1 per 1000 to 2000 epileptic patients has been reported (Vizioli 1962; Nagaraja and Chand 1984). The unusually high figures reported for Sri Lanka (Senanayake 1990) seem related to an idiosyncratic definition and to ascertainment methods.
It is our impression that patients with eating epilepsy and extralimbic seizure onset are more sensitive to either somatosensory or proprioceptive stimuli during eating and are more likely to report that seizure induction can be prevented by altering the sensory characteristics of their food. Some will drink through a straw rather than from a cup or avoid biting into a whole fruit by cutting it into small pieces. Stimulus alteration can reduce seizure frequency in what can otherwise be an intractable or socially disabling condition. Some patients take advantage of a refractory postictal period by inducing a seizure to avoid a later attack in an embarrassing setting. Drugs effective for partial seizures are necessary but medically intractable cases should be recognized early and assessed for surgical treatment.
Precipitating Stimuli for Reflex Seizures