Summary:Purpose: Headache is often ignored as a symptom of epileptic seizures. The purpose of this prospective study was to analyze frequency, classification, and characteristics of seizure-associated headache (SH) according to the criteria of the International Headache Society.Methods: Over a period of 15 months, 341 patients with epilepsy, consecutively evaluated at our outpatient clinic for SH, completed a standardized questionnaire.Results: Of the 341 epilepsy patients, 115 (34%) experienced SH with a pain intensity of 6.1 ± 1.6 (SD) on the visual analogue scale and a duration of 12.8 ± 15.7 (SD) h. Seizures were always accompanied by headache in 69 (60%) of these 115 patients. SH occurred in four (3%) of 115 patients only preictally, in 31 (27%) of 115 patients periictally, and in 80 (70%) of 115 patients only postictally. In the majority of the 115 patients (55.7%), SH could be classified as migraine headache, whereas in 36.5%, as tension-type headache. The type of SH was not correlated with sex, an epilepsy syndrome, or a seizure type. Migraine-like SH was significantly associated with a history of migraine (p < 0.001). In 20 (77%) of the 26 patients experiencing migraine-like SH with a history of migraine, the phenomenology of migraine-like SH and migraine attacks was identical.Conclusions: SH is a frequent, long-lasting, and severe symptom of epileptic seizures, causing major impairment of daily living. A history of migraine significantly increases the risk for developing migraine-like SH.
The gabapentinoids gabapentin and pregabalin have been related to addiction citing pharmacovigilance data, some case presentations and increasing reports mainly from methadone maintenance treatment programs or emergency medicine. Most of these reports were based on patients with another current or previous substance use disorder (SUD). According to the ICD-10 dependence criteria, physical dependence (withdrawal symptoms, tolerance) was reported most frequently alongside regular use of gabapentinoids. Far less patients showed key symptoms of behavioral dependence (craving, loss of control, or addictive behavior). Through a literature review, we found 2 and 13 case reports about gabapentionoid-seeking behavior or craving for gabapentin and pregabalin, respectively. Those patients without a history of another SUD, but being behaviorally dependent on gabapentinoids, deemed more appropriate to reflect the true addictive power of these drugs. We found solely 4 such cases, all referring to pregabalin and none for gabapentin. Taking into account that gabapentinoids have become widely distributed and easily obtainable via the internet or black-markets, one would expect many more of these cases, if gabapentinoids had considerable addictive power. Moreover, we are not aware of any patient who sought detoxification treatment owing to the misuse of gabapentinoids. Unlike for traditional psychoactive drugs, there is only very scarce evidence for gabapentinoids to be misused in a long-term manner and to be rewarding and reinforcing in animal experiments. Further, we assessed the hazardous potential of gabapentin and pregabalin in relation to that of traditional substances of abuse. Altogether, we support the view that gabapentinoids are quite rarely addictive in the general population. In patients with a history of SUD, however, gabapentinoids (notably pregabalin) should avoided or, if thought to be beneficial, administered with caution by using a strict prescription and therapy monitoring.
No specific epileptic characteristics could be found in patients with comorbidity. Altered cerebral excitability resulting in an increased occurrence of spreading depression may explain the differences in migraine attacks in patients with comorbidity as compared to patients with migraine alone.
BackgroundIt is unusual for purpura to emerge as a result of drinking alcohol. Such a peculiarity was observed in a 55-year-old man with a 30-year history of heavy alcohol use.Case presentationThe Caucasian patient was studied for 11 years during several detoxification treatments. During the last 2 years of that period, purpuric rashes were newly observed. The asymptomatic purpura was limited to both lower limbs, self-limiting with abstinence, and reoccurring swiftly with alcohol relapse. This sequence was observed six times, suggesting a causative role of alcohol or its metabolites. A skin biopsy revealed histological features of purpura pigmentosa progressiva (termed Schamberg’s disease). Additionally, alcoholic fatty liver disease markedly elevated serum immunoglobulins (immunoglobulin A and immunoglobulin E), activated T-lymphocytes, and increased C-reactive protein. In addition, moderate combined (cellular and humoral) immunodeficiency was found. Unlike the patient’s immunoglobulin A level, his serum immunoglobulin E level fell in the first days of abstinence, which corresponded to the time of purpura decline. Systemic vasculitis and clotting disorders were excluded. The benign character of the purpura was supported by missing circulating immune complexes or complement activation. An alcohol provocation test with vinegar was followed by the development of fresh “cayenne pepper” spots characteristic of Schamberg’s disease.ConclusionsThis case report demonstrates that Schamberg’s disease can be strongly related to alcohol intake, in our patient most likely as a late complication of severe alcoholism with alcoholic liver disease. Immunologic disturbances thereby acquired could have constituted a basis for a hypersensitivity-like reaction after ingestion of alcohol. Schamberg’s disease induction by vinegar may point to an involvement of acetate, a metabolite of ethanol.
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