Epilepsy and Behavior Case Reports最新文献

We report a child with Lennox–Gastaut syndrome with an increase in seizure frequency and loss of psychomotor skills due to a disintegrated cervical VNS lead, not detected during standard device monitoring. The lead was completely removed and replaced by a new 303 lead on the same nerve segment. After reinitiating VNS, side effects forced us to switch it off, resulting in immediate seizure recurrence. EEG recording demonstrated a non-convulsive status epilepticus that was halted by reinitiating VNS therapy. Thereafter, he remained seizure free for eight months, and regained psychomotor development.

Vomiting is a typical symptom of cerebellar hemorrhage. Usually only supportive care such as antiemetic drugs are available. A 76-year-old woman presented in a light coma. A head CT demonstrated right cerebellar hemorrhage and the hematoma was surgically evacuated. Her intractable vomiting started 3 weeks after surgery. Because her vomiting was unexplained, we checked her EEG, which demonstrated generalized periodic discharges. We diagnosed her with ictal vomiting. Anti-seizure medication was administered and vomiting was rapidly controlled. In conclusion, physicians must be aware that vomiting may rarely occur as a sign of seizures and status epilepticus.

Numerous autoantibodies are implicated in the pathogenesis of autoimmune epilepsy. In the past decade, many case series reported the association of glutamic acid decarboxylase 65 (GAD 65) antibodies with epilepsy. Conjoint presence of GAD 65 antibodies with antinuclear, anti-thyroid, and anti-parietal cell antibodies has often been demonstrated. However, concomitant elevated levels of GAD 65 and P/Q voltage gated calcium channel (VGCC) antibodies is rare. We report a case of autoimmune epilepsy with conjoint GAD 65 and P/Q VGCC antibodies in the absence of malignancy. This report highlights a possible role of P/Q VGCC antibodies in the pathogenesis of autoimmune epilepsy.

Objectives

To match responsive neurostimulator (RNS) and polysomnographic data to determine if RNS detections and stimulations correlate with measurements of sleep disordered breathing and continuous glucose measurements (CGM).

Materials and methods

In a patient with an RNS with detection/stimulation leads implanted bi-temporally detection-stimulation counts were matched by time with coinciding polysomnogram and CGM data.

Results

Temporal dispersion of RNS DSC were independent of measures of sleep apnea, hypopnea or glucose.

Conclusion

Hippocampal nighttime responsive neurostimulation therapies did not appear to worsen measures of normal or abnormal sleep.

The association between emotional stimuli and temporal lobe epilepsy (TLE) is largely unknown. Here, we report the case of a depressed, 50-year-old female complaining of episodes of a “spaced out” experience precipitated by emotional stimuli. Psychogenic non-epileptic attacks were suspected. However, video-EEG coupled with emotional stimuli-provoked procedures and MRI findings of amygdala enlargement, led to the diagnosis of left TLE. Accurate diagnosis and explanation improved her subjective depression and seizure frequency. This case demonstrated that emotional stimuli can provoke seizures in TLE and suggested the involvement of the enlarged amygdala and the modulation of emotion-related neural circuits.

Purpose

To identify risk factors for VNS-associated arrhythmia.

Methods

A literature review identified 14 papers with 21 patients. We compared patients with VNS associated arrhythmia (arrhythmia group, n = 22) and patients without VNS associated arrhythmia (control group of our VNS implanted patients, n = 29).

Results

New onset syncopal events following VNS placement were seen in the arrhythmia group (p < 0.001).

Conclusion

Even though arrhythmia could be symptomatic, most cases associated with syncope were treated as new-onset epileptic seizures with adjustment of anti-seizure drugs. To detect cardiac asystole during VNS treatment, clinicians should be alert to the possibility of new onset syncopal events that differ from habitual seizures.

Background

A ketogenic diet (KD) may have a role in treating patients in super-refractory status epilepticus (SRSE). Sodium-glucose cotransporter 2 (SGLT2) inhibitors have a risk of ketoacidosis that could facilitate induction of KD.

Case summary

A 42-year-old with a history of drug resistant epilepsy developed SRSE requiring several pharmacological interventions during her hospital course including the initiation of KD that failed. SGLT2 inhibitor therapy was initiated in a successful attempt to augment ketone production.

Conclusion

SGLT2 inhibitors may have a therapeutic value in SRSE patients who cannot achieve ketosis with KD alone.

Cardiopulmonary complications associated with epilepsy are generally associated with generalized tonic–clonic seizures, as a consequence of systemic adrenergic discharge and release of inflammatory mediators. We present a case of a 34-year-old woman with a history of Focal epilepsy since adolescence, who presented self-limited pulmonary edema following a focal to bilateral tonic–clonic seizure with subsequent resolution of the symptoms. We also made a brief review of neurogenic pulmonary edema, its proposed pathophysiology, treatment and its relation with sudden unexpected death in epilepsy (SUDEP).