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Alcohol-Responsive Epilepsia Partialis Continua

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Alcohol-Responsive Epilepsia Partialis Continua Journal Identification = EPD Article Identification = 0626 Date: March 21, 2014 Time: 12:25 pm Clinical commentary with video sequences Epileptic Disord 2014; 16 (1): 107-11 Alcohol-responsive epilepsia partialis continua Trevor A Steve, Donald W Gross Division of Neurology, Department of Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada ABSTRACT – Epilepsia partialis continua is typically associated with lesions of the cerebral cortex. However, subcortical lesions can also cause this condition. We present a patient with epilepsia partialis continua who failed to respond to conventional anticonvulsant medications but experienced a dramatic transient response to alcohol and a subsequent response to primidone. This pattern of sensitivity, which is similar to that seen in essen- tial tremor, has led to the hypothesis that the two disorders are associated with pathology within the same anatomical network. A new pathophys- iological model is thus proposed for the occurrence of epilepsia partialis continua in both cortical and subcortical disease processes. [Published with video sequences] Key words: epilepsia partialis continua, myoclonus, essential tremor, tremor Epilepsia partialis continua (EPC) both cortical and subcortical lesions is defined as “continuous muscle (Guerrini, 2009). jerks of cortical origin” (Cockerell Essential tremor (ET) consists of et al., 1996). Patients with EPC postural-kinetic hand tremor and suffer from infrequent generalised variable involvement of other body seizures and medically intractable regions. A striking feature in ET myoclonic jerks. The most com- is a dramatic temporary response mon causes of EPC are Rasmussen’s of the tremor to alcohol. Many encephalitis, tumours, stroke, and patients also experience a moder- focal cortical dysplasia. ate to marked improvement with The pathophysiology of EPC is primidone (Elble, 2009). The patho- incompletely understood (Guerrini, physiology of ET is believed to 2009). It is typically associated with involve “tremorogenic oscillation lesions in the contralateral cerebral and synchrony in motor networks”, cortex (Cockerell et al., 1996). How- involving the inferior olive, cere- ever, subcortical pathology can also bellum, and cerebral cortex (Elble, cause EPC (Juul-Jensen and Denny- 2009). We report a case of EPC Correspondence: Donald W Gross Brown, 1966). The role of subcortical which was alcohol and primidone 2E3.19 Walter Mackenzie Health Sciences structures in maintaining cortical responsive. Given the similarities Centre, epileptic activity remains unclear. of pharmacological sensitivity, we 8440 112 St NW, Presently, “no single mechanism” hypothesize overlap in the anatom- Edmonton T6G 2B7, Canada has been proposed to account ical network involved in ET and <[email protected]> for the occurrence of EPC with EPC. doi:10.1684/epd.2014.0626 Epileptic Disord, Vol. 16, No. 1, March 2014 107 Journal Identification = EPD Article Identification = 0626 Date: March 21, 2014 Time: 12:25 pm T.A. Steve, D.W. Gross Case Study that after having consumed several alcoholic bever- ages, his EPC resolved acutely and his hand function In 1998, a 31-year-old, right-handed male developed essentially improved to normal. At this time, he was new onset of continuous twitching of his right middle able to pick up a grain of rice with chopsticks, some- finger. The movements remained restricted to this thing that would have been impossible in his prior finger and were not accompanied by alteration of con- state. The next morning, his EPC had not only returned, sciousness. The patient did not seek medical attention but transiently worsened. and the twitching resolved spontaneously after three Based on the patient’s report of alcohol responsive- weeks. ness, primidone was started at a dose of 125 mg daily. The twitching returned again without provocation Within days of starting on this medication, after nearly in 2004. Over the course of five days, the move- seven years of continuous EPC, his movements com- ments spread sequentially to contiguous fingers and pletely disappeared. In association with this, his right the hand, and the patient then had a generalised hand function again improved dramatically (he was seizure lasting two minutes. Following the generalised able to shave with his right hand). After approximately tonic-clonic convulsion, the patient continued to have one week, the movements returned. constant rhythmic twitching of the right arm (video With increasing doses of primidone, both the EPC sequence). His right upper extremity was rendered and motor function improved, but complete con- non-functional by the movements. Initial treatment trol was not obtained. A trial of propranolol had with valproic acid, carbamazepine, and phenytoin was no effect on the movements, suggesting peripheral unsuccessful. Clonazepam and levetiracetam were mechanisms did not play a major role in our patient partially effective, but despite these medications, the (Elble, 2009). Ethosuximide, which acts via inhibi- movements persisted. tion of low-threshold (T-type) calcium channels, also The EEG showed continuous rhythmic delta activ- had no effect on the movements. Based on reports ity in the left frontal-central-parietal region. An MRI of alcohol-responsive myoclonus responding well to performed the day following his generalised convul- gamma-hydroxybutyrate, this medication was tried for sion showed a focal region of increased T2 signal in one week (Frucht et al., 2005). The patient reported the left hemisphere, adjacent to the precentral sul- worsening of EPC during this trial as well as excess cus (figure 1A). This region demonstrated restricted sedation, and the medication was therefore discon- diffusion but not gadolinium enhancement. The CSF tinued. His current medications are levetiracetam at examination showed no cells and normal protein. 500 mg once daily, oxcarbazepine at 600 mg twice daily, As the continuous focal motor seizures failed to clonazepam at 0.5 mg twice daily, and primidone at respond to anticonvulsants, aggressive management 375 mg twice daily. He presently remains disabled by was attempted. A sedating dose of intravenous propo- continuous twitching of the right hand and is unable fol eliminated the movements, but they returned when to write or shave. the infusion was discontinued. Propofol and pento- barbital in combination were then titrated to burst suppression, and the patient was maintained in coma Discussion for 48 hours. During this time, EPC was again abolish- ed, but the movements recurred immediately after dis- This report describes a patient with severe medically continuation of the anaesthetic. intractable EPC. Investigation revealed a transient The patient continued to have EPC over the next T2 hyperintensity adjacent to the left precentral several years. Some benefit was noted with topiramate, sulcus, likely related to ongoing seizure activity in but this medication was stopped due to development a location typical for EPC (Cockerell et al., 1996). of kidney stones. Oxcarbazepine was partially effec- Follow-up imaging ruled out stroke and tumour as tive and was continued. No significant improvement diagnostic possibilities. The negative cerebrospinal was achieved despite treatment with lacosamide, intra- fluid examination made encephalitis unlikely. The age venous solumedrol, and the modified Atkin’s diet. of presentation is atypical for focal cortical dysplasia. He suffered his only additional generalised seizure The patient did not develop progressive hemispheric in 2006. EPC remained essentially continuous and was atrophy characteristic of adult-onset Rasmussen’s, associated with major functional impairment of the use and did not respond to a course of corticosteroids. of his right hand. Repeat MRI in 2010 demonstrated Therefore, the underlying aetiology of EPC in this case atrophy of the cerebral cortex adjacent to the pre- remains uncertain. central sulcus, without evidence of T2 hyperintensity The response to alcohol and primidone in this patient (figure 1B). was dramatic, resulting in temporary, complete reso- In July of 2011, the patient presented to the clinic lution of EPC, and requires mechanistic explanation. having made an unusual observation. He recounted Primidone does have anticonvulsant effects, but the 108 Epileptic Disord, Vol. 16, No. 1, March 2014 Journal Identification = EPD Article Identification = 0626 Date: March 21, 2014 Time: 12:25 pm Alcohol-responsive EPC A B Figure 1. (A) Initial fluid-attenuated inversion recovery (FLAIR) brain MRI showing increased T2 signal in the cerebral cortex adjacent to the left precentral sulcus. (B) Follow-up FLAIR brain MRI performed six years later showing resolution of T2 signal abnormality and cortical atrophy adjacent to the precentral sulcus. patient was refractory to AEDs which act by various and primidone is believed to act in a similar fashion mechanisms. Given the limited response of the EPC (Elble, 2009). Firstly, alcohol is capable of blocking to conventional anticonvulsants, we hypothesize that T-type calcium channels in the inferior olive (Sinton alcohol and primidone most likely acted in this patient et al., 1989). These channels are thought to be integral via a similar mechanism to that in Essential Tremor (ET). to the pathophysiology of ET by setting up excessive Animal studies have suggested that alcohol eliminates excitation of cerebellar Purkinje cells via the climbing ET by three mechanisms (Mostile and Jankovic, 2010), fibres (Mostile and Jankovic,
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