This study aimed to investigate the clinical predictors of post-ictal headache (PIH) in patients with epilepsy in a tertiary center in Brazil. Methods: 302 individuals with adult-onset epilepsy were followed for 9.8 years in our Hospital. Structured questionnaires about headaches were applied. The presence of PIH was the primary outcome. We used multilevel linear modeling in our data analysis. Results: From the total, 46.3% had post-ictal headaches. Tension-type post-ictal headache was present in 55% (N = 77) of the subjects, migrainous in 32.1% (N = 45), and both types in 12.8% (N = 18). Family history of migraine (Odds ratio: 1.696; 95% CI: 1.372 to 2.096), diagnosis of drug-resistant epilepsy (Odds ratio: 1.169; 95% CI: 1.135 to 2.146), months since last visit (Odds ratio: 1.464; 95% CI: 1.243 to 2.888), and generalized seizure onset type of epilepsy (Odds ratio: 1.527; 95% CI: 1.114 to 1.668), were significant determinants of PIH on multilevel linear modeling. Discussion: PIH are associated with drug-resistant epilepsy, generalized seizures, and family history of migraine. The rates of pos-ictal headaches could be influenced by the use of antiepileptic drugs.
Introduction: Jarisch-Herxheimer reaction (JHR) is defined as a transient immunologic reaction, classically seen in patients during syphilis treatment. JHR is a rare cause of status epilepticus (SE) in neurosyphilis. We describe a case of generalized convulsive SE (GCSE) probably secondary to JHR in a patient with neurosyphilis. Case Report: A 23-year-old man presented with progressive behavioral changes with 4 months of onset and pupillary alteration with 9 months of onset. He had experienced blurred vision and had noticed mydriasis in the left eye. Brain magnetic resonance imaging was normal; however, sexually transmitted infections were not investigated. After 1 month, the blurred vision disappeared, but mydriasis remained. Three months passed, and he reported progressive behavioral changes. Laboratory tests were within the normal limits, except by positive blood venereal disease research laboratory. Later, the cerebrospinal fluid analysis was requested, which revealed a positive venereal disease research laboratory. Electroencephalogram and brain magnetic resonance imaging were normal. Treatment was started with crystalline penicillin G. A GCSE began 12 hours after the first dose of penicillin. He did not develop classic signs and symptoms of the JHR. An EEG showed periodic lateralized epileptiform discharges. Conclusions: To the author’s knowledge, there are 3 cases in the literature of nonconvulsive SE with JHR in neurosyphilis, and the present report was the first to describe the occurrence of GCSE secondary to JHR in neurosyphilis. Another important finding, in this case, was the isolated unilateral mydriatic tonic pupil, rarely reported as an early isolated symptom of neurosyphilis. In this way, it is essential that patients presenting with isolated unilateral tonic pupil receive an adequate investigation for syphilis.
Fahr's disease (FD) is a rare inherited or sporadic disorder characterized by symmetrical calcium deposits in the basal ganglia and dentate nuclei with the absence of biochemical abnormalities. Clinical manifestations can start at different ages with a variety of presentations. We report a case of a 68-year-old male who presented to our service with clinical signs and symptoms of pure and progressive dementia. Afterward, he developed mood changes, and finally, movement disorders, probably due to a sporadic form of FD. Noncontrast cranial computed tomography scan demonstrated scattered brain parenchyma, bilateral calcifications in the basal ganglia, and dentate nuclei. Standard blood tests were within the normal limits. In this way, FD can present with pure dementia at onset, reflecting a wide range of neurological manifestations. The diagnosis is challenging, and we proposed an acronym to facilitate the learning of the diagnostic criteria.
Cerebellar atrophy can be found with long-term phenytoin (PHT) use or acute phenytoin intoxication. PHT may cause cerebellar symptoms, such as nystagmus, diplopia, dysarthria and ataxia. Clinical manifestations may be persistent. We report a case of a 41-year-old male who presented with cerebellar dysfunction and cerebellar atrophy after longterm phenytoin use. He had ataxic gait, preserved strength, commuting deep reflexes, dysmetria, dysdiadochocinesia, scanning speech and somnolence. Cranial computed tomography revealed enlargement of interfollicular cerebrospinal fluid spaces in cerebellum and also a slight enlargement of the fourth ventricle, suggesting signs of cerebellar volumetric reduction. PHT was withdrawn. Six months later, he presented improvement in his condition; he had atypical gait, mild dysmetria, diadochokinesia and normal speech. In conclusion, clinicians should be vigilant with patients on phenytoin. If the patient has cerebellar signs with a correspondent clinical history of phenytoin intoxication CT scan should be helpful as an initial cerebellar assessment.
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