OBJECTIVE:To describe the chiropractic management of a patient presenting with complaints of low back pain and epileptic seizures. The discussion also addresses epilepsy and the current concepts of this disorder; possible mechanisms for the neurological effects of the chiropractic adjustment at sites of subluxation and its therapeutic implications are proposed.

CLINICAL FEATURES:A 21-year-old woman with low back pain reported that she had fainted during the night and hit her head. She had been diagnosed since childhood with grand mal (tonicclonic) seizures as well as petit mal seizures. She had a seizure approximately every 3 hr, with a duration between 10 sec and 30 min for each episode. Examination indicated signs of subluxation/dysfunction at the L5-S1, C6-C7 and C3-C4 spinal levels. There was no evidence of cranial nerve involvement or any upper motor neuron lesion. Radiographic analysis revealed retrolisthesis of L5, hypolordosis of the cervical spine and hyperextension of the C6-C7 motion segment.

INTERVENTION AND OUTCOME:Chiropractic adjustments using a specific-contact, short-lever arm, high-velocity, low-amplitude maneuver (i.e., Gonstead) were applied to the subluxations at the cervical, thoracic and lumbopelvic region. The patient's reported low back pain and neck complaints improved and her seizure frequency decreased. At 1.5-yr follow-up, the patient reported her low back complaints had resolved and her seizures had decreased (period between seizures as great as 2 months).

CONCLUSION:Results encourage further investigation of possible neurological sequalae, such as epileptic seizures, from spinal dysfunction identified as vertebral subluxation complexes by chiropractors and treated by specific spinal adjustments.

The effect of Sahaja yoga meditation on seizure control and electroencephalographic alterations was assessed in 32 patients of idiopathic epilepsy. The subjects were randomly divided into 3 groups. Group I (n = 10) practised Sahaja yoga for 6 months, Group II (n = 10) practised exercises mimicking Sahaja yoga for 6 months and Group III (n = 12) served as the epileptic control group. Group I subjects reported a 62 per cent decrease in seizure frequency at 3 months and a further decrease of 86 per cent at 6 months of intervention. Power spectral analysis of EEG showed a shift in frequency from 0-8 Hz towards 8-20 Hz. The ratios of EEG powers in delta (D), theta (T), alpha (A) and beta (B) bands i.e., A/D, A/D + T, A/T and A + B/D + T were increased. Per cent D power decreased and per cent A increased. No significant changes in any of the parameters were found in Groups II and III, indicating that Sahaja yoga practice brings about seizure reduction and EEG changes. Sahaja yoga could prove to be beneficial in the management of patients of epilepsy.

OBJECTIVE:The mechanisms of the ketogenic diet remain unclear, but several predictors of response have been proposed. We aimed is to study the relationship between the etiology of epilepsy, cerebrospinal fluid neurotransmitters, pterins, and amino acids, and response to a ketogenic diet.

METHODS:We studied 60 patients who began classic ketogenic diet treatment for refractory epilepsy. In 24 of 60 individuals, we analyzed cerebrospinal fluid neurotransmitters, pterins, and amino acids in baseline conditions. Mean age at epilepsy onset was 24 months, 83.3% were focal epilepsies, and in 51.7% the etiology of the epilepsy was unknown.

RESULTS:Six months after initiating the ketogenic diet, it was effective (greater than a 50% reduction in seizure frequency) in 31.6% of patients. We did not find a link between rate of efficacy for the ketogenic diet and etiologies of epilepsy, nor did we find a link between the rate of efficacy for the ketogenic diet and cerebrospinal fluid pterins and biogenic amines concentrations. However, we found statistically significant differences for lysine and arginine values in the cerebrospinal fluid between ketogenic diet responders and nonresponders, but not for the other amino acids analyzed.

SIGNIFICANCE:The values of some amino acids were significantly different in relationship with the ketogenic diet efficacy; however, the epilepsy etiology and the cerebrospinal fluid biogenic amine and pterin values were not.

The ketogenic diet (KD) is used for the treatment of refractory epilepsy in children, however, the mechanism(s) remains largely unknown. Also, the antiepileptogenic potential in animal models of epilepsy has been poorly addressed. Activation of cannabinoid type-1 receptor (CB(1)-R) upon seizure activity may mediate neuroprotection as may several N-acylethanolamines. It is unknown how the KD interfere with the endocannabinoid system. We investigated the antiepileptogenic potential of the KD in the pentylenetetrazole kindling model in young mice and measured the hippocampal levels of CB(1)-R by Western blot and of endocannabinoids and N-acylethanolamines by mass spectrometry. The KD significantly decreased incidence and severity of seizures, and significantly increased the latency to clonic convulsions. There were no changes in levels of endocannabinoids or CB(1)-R expression by either seizure activity or type of diet. The level of oleoylethanolamide as well as the sum of N-acylethanolamines were significantly decreased by the KD, but were unaffected by seizure activity. The study shows that the KD had clear antiepileptogenic properties in the pentylenetetrazole kindling model and does not support a role of endocannabinoids in this model. The significance of the decreased hippocampal level of oleoylethanolamide awaits further studies.

WHAT IS KNOWN AND OBJECTIVE:Antiepileptic drugs often produce serious adverse effects, and many patients do not respond to them properly. Phytocannabinoids produce anticonvulsant effects in preclinical and preliminary human studies, and appear to produce fewer adverse effects than available antiepileptic drugs. The present review summarizes studies on the anticonvulsant properties of phytocannabinoids.

METHODS:Literature search using the PubMed database to identify studies on phytocannabinoids and epilepsy.

RESULTS AND DISCUSSION:Preclinical studies suggest that phytocannabinoids, especially cannabidiol and cannabidivarin, have potent anticonvulsant effects which are mediated by the endocannabinoid system. Human studies are limited in number and quality, but suggest that cannabidiol has anticonvulsant effects in adult and infantile epilepsy and is well tolerated after prolonged administration.

WHAT IS NEW AND CONCLUSION:Phytocannabinoids produce anticonvulsant effects through the endocannabinoid system, with few adverse effects. Cannabidiol and cannabidivarin should be tested in randomized, controlled clinical trials, especially in infantile epileptic syndromes.

OBJECTIVE:To evaluate the efficacy and safety of the ketogenic diet (KD) in infants (<1.5 years of age) compared with older children.

METHODS:Patients with complete follow-up data of≥3 months after initiation of the KD were analyzed retrospectively. Infants<1.5 years at initiation of the KD (Group A) were compared with children>1.5 years (Group B).

RESULTS:127 children were screened, 115 (Group A: 58/Group B: 57) were included. There were no significant differences between groups with respect to responder rates (63.8% vs. 57.9% at 3 months), but more infants became seizure free (34.5% vs. 19% at 3 months; 32.7% vs. 17.5% at 6 and 12 months). This result remained stable also after termination of the KD (30.6% vs. 3.9% at last follow-up) (p=0.000). Looking at infants<9 months of age separately (n=42), this result was even stronger with significantly more infants being seizure free at 6 and at 12 months (p=0.005, p=0.014, respectively). In addition, a significantly higher number of infants remained seizure free in the long-term (p=0.001). No group differences between infants and children with respect to safety were observed. Overall 52/115 patients (45.21%) reported side effects, but withdrawal of the KD was only necessary in one infant. Acceptance of the KD was better in infants compared with children at 3 months (0 vs. 14, p=0.000), but became difficult when solid food was introduced (16 vs. 14; n.s.).

SIGNIFICANCE:According to our results, the KD is highly effective and well tolerated in infants with epilepsy. Seizure freedom is more often achieved and maintained in infants. Acceptance of the diet is better before the introduction of solid food. Therefore, we recommend the early use of the KD during the course of epilepsy.

Although the ketogenic diet has been used in the therapy for epilepsy for more than 50 years, there are few studies concerned with the effects of this diet on the central nervous system. Recent attempts to unravel the biochemical effects of the ketogenic diet on the brain seem to be a fruitful approach to understanding how the ketogenic diet causes anticonvulsant effects. Another exciting approach is the development of animal models in which various effects of the diet can be correlated with changes in seizure protection. It would be useful to determine whether the diet produces any neurophysiological effects that could account for some, or all, of its antiseizure properties. Finally, the efficacy of the diet is impressive. It is likely that the ketogenic diet will never be of major therapeutic importance because of the expense and commitment required of the patient and the family. Nevertheless, it appears obvious that continued study of a therapy which seems to work so well will give us some valuable clues as to the mechanism of seizures and their control. Further investigations into the mechanism of action of the ketogenic diet should be encouraged.