Many patients with ME experience seizures, some of which may not be immediately recognisable.
The types of seizures persons with ME get are notoriously difficult to detect on a normal EGC and often they get confused with psychiatric behaviour. They can be feelings of everything being unreal or dreamlike, losing control of thoughts or having the same thoughts going round and round, laughing or weeping uncontrollably, making sounds without meaning to and there are seizures which involve making bizarre uncontrollable movements, without losing consciousness.
The most common symptoms of focal seizures in the frontal lobes
It is difficult to deny the intriguing possibility that some abnormal mental states (in epilepsy) are due to prolonged seizure activity. Although there is undisputed evidence that prolonged epileptiform EEG discharges (characteristic of status) in hippocampal and amygdaloid regions can be associated with behavioral abnormalities and can occur with or without clear-cut scalp EEG changes, it is quite unknown to what extent the generality of "interictal behavioral peculiarities" might be associated with such "subclinical EEG status activity" in deep structures.
Since limbic status epilepticus implies seizure discharges in the limbic system, it is not surprising that without intracranial recording from the core structures of the limbic system, such as hippocampal formation and amygdala, limbic status epilepticus is often not detectable. This might be one reason that limbic status epilepticus is rarely reported in literature in comparison to generalized convulsive status epilepticus and absence status epilepticus.
Time distortion, depersonalization, and disorientation are types of cognitive seizures or dyscognitive seizures (2.3) that have all been ascribed to the parahippocampal or fusiform gyri (70). Forced thoughts of a repetitive nature, with or without pressured speech, can be seen in some frontal lobe seizures (71). In this section, we deal with those seizures affecting attention and language. Seizures involving mood or affect (affective; 188.8.131.52), memory (mnemonic; 184.108.40.206), or distorted perceptions (illusory – 220.127.116.11) are dealt with under the section on Psychic Seizures. These are all listed under experiential (2.2.2) in the newly proposed ILAE classification (1)
This paper describes how any frontal lobe seizure can be continuous and last for months if not years.
Complex partial status epilepticus of frontal lobe origin. Takeda A. (1988)
Abstract: Nonconvulsive status epilepticus may be subdivided into generalized (absence) status and complex partial status. The latter is generally considered as a rare condition, whereas the former is fairly common to have been reported in many articles. We have reported here a case of complex partial status epilepticus in which the seizure origin was thought to be located in the frontal but not temporal lobe. After looking over the relevant literatures we commented that the incidence of complex partial status of extratemporal origin does not seem to be as rare as it has been believed to be. The main reason for this is the frequency with which it is misdiagnosed. The diagnostic errors are due to a failure to recognize the epileptic cause of the attacks or to appreciate localizing the clinical seizure characteristics and misleading scalp EEG findings. By making a closer observation of clinical manifestations, the likelihood that a correct diagnosis can be made will be increased.
Focal (partial) seizures in the frontal lobes
Focal seizures starting in the frontal lobes are common.
Your frontal lobes are responsible for many different functions. These include movement, emotions, memory, language, and social and sexual behaviour. The frontal lobes are also considered to be home to your personality.
Not all frontal lobe seizures will be noticed by an onlooker. However, some frontal lobe seizures can look quite dramatic and unusual. Because of this it is common for them to be wrongly diagnosed as something other than epilepsy.
The most common symptoms of focal seizures in the frontal lobes
This looks at the role of glutamate and the NMDA receptor as the cause of limbic seizures in Epilepsy.
Psychic epileptic seizures involve purely sensory or subjective symptoms with retained memory for the ictus. These seizures do not involve loss of consciousness. They do not have a motor component. Thus, some psychic seizures have been previously covered in the sections on sensory symptomatology and dyscognitive seizures. In this section, we discuss ictal symptoms including hallucinations of all modalities, illusions involving distortions of existing objects, dysmnesic symptoms involving distortions of time, and intellectual symptoms with alterations in thought content. Psychic seizures must be distinguished from the psychiatric illnesses that they may closely resemble.
The role of glutamate in epilepsy and other CNS disorders. BS Meldrum (Neurology, 1994)
Glutamate is the principal excitatory neurotransmitter in the brain and, as such, it inevitably plays a role in the initiation and spread of seizure activity. It also plays a critical role in epileptogenesis. The process of "kindling" limbic seizures in rodents by repeated electrical stimulation is dependent on activation of N-methyl-D-aspartate (NMDA) receptors. The function of these receptors is enhanced in the hippocampus of kindled rats and in the cerebral cortex of patients with focal epilepsy. Microdialysis studies show an increase in the extracellular concentration of glutamate and aspartate before or during seizure onset, suggesting that either enhanced amino acid release or impaired uptake contributes to seizure initiation. Glutamate antagonists selective for NMDA or non-NMDA receptors are potent anticonvulsants when given systemically in a wide variety of animal models of epilepsy. They are of limited efficacy against kindled seizures in rats and (on the basis of preliminary evidence) in patients with drug-refractory complex partial seizures. Cognitive side effects appear to be a significant problem with competitive, as well as noncompetitive, NMDA antagonists. Glutamate receptor antagonists provide significant protection against brain damage following global or focal cerebral ischemia or acute traumatic injury in rodent models. Anticonvulsant compounds of the lamotrigine type, which act on sodium channels and reduce ischemia-induced glutamate release, are cerebroprotective in rodent ischemia models and are free from the cognitive side effects of NMDA-receptor antagonists.