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    12 views7 pages

    Post Stroke Seizure

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    hadiatussalamah

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    SECTION FDITOR: DAVID E PLEASURE. MD Poststroke Seizures Isaac E. Silverman, MD; Lucas Restrepo, MD; Gregory C. Mathews, MD, PhD troke is the most common cause of seizures in the elderly, and seizures are among the most common neurologic sequelae of stroke. About 10% of all stroke patients experience sei- zures, from stroke onset until several years later. This review discusses current understand- ing of the epidemiology, pathogenesis, classification, clinical manifestations, diagnostic stud- ies, differential diagnosis, and management issues of seizures associated with various cerebrovascular lesions, with a focus on anticonvulsant use in the elderly: Arch Neurol. 2002;59:195-202 EPIDEMIOLOGY In population studies, stroke is the most commonly identified cause of epilepsy in adult populations older than 35 years." In the elderly, stroke accounts for more than half of the newly diagnosed cases of epi- lepsy in which a cause is determined, ahead of degenerative disorders, brain tumors, and hhead trauma.’ From stroke registry data shout 59% to 20% of ll individuals who have stroke will have subsequent seizures but epilepsy (recurrent seizures) will develop {monly a small subset of this group. Given that, in each year, more than 730000 people im this country have a stroke, a conserva- Uiveincidence of seizures alter stroke is about 36500 new cases per year The largest and most rigorous meth- odological attempt to examine poststroke seizures was the prospective mullicenterre- port from the Seizures After Stroke Study Group. The study enrolled 1897 patients and found an overall incidence of seizures of 8.0%, Recurrent seizures consistent with the development of epilepsy wet curring in 25% ofthe patients, but the mean follow-up was only 9 month Seizures may bea more common ac- companiment of hemorrhagie rather than ischemic stroke. bladin ct al found the incidence of sei sures tobe 10,6%among 265 patients with sntracerebral hemorehage vs 86% among 1632 with ischemic stroke. Ia another prospective series,’ seizures occurred in 444% of 1000 patients, including 15.43% ith lobar or extensive intracerebral hemor- rhage, 8.5% with subarachnoid hemor hage, 6.5% with cortical infarction, and 3.7% with hemispheric transient ischemic altacks. 4 seizure was the presenting ( ture of intracranial hemorrhage in 30% of 1402 patients Among 95 patients with an- curysmnal subarachnoid hemorrhage, the fncidence rate of prchospital seizures was higher (17.9%) than that occuring i the hospital (4.19%)." CLASSIFICATION AND. PATHOGENESIS Seizures after stroke are classified as early or late onset, according to their timing af ter brain ischemia, ina paradigm compa- rable to post-traumatic epilepsy.*7 An arbitrary cut point of 2 weeks after the pre- senting stroke has been recognized to dis- nguish between early- and late-onset poststroke seizures.”"® Different charac- {eristics and mechanisms of poststroke se ures, according to their proximity to the onset of brain ischemia, have heen pro- posed, but no clear pathophysiologtcal basis exists for the 2-week cut point Most early-onset seizures occur dur- ing the first 1 to 2days after ischemia. Al- From The Stroke Center at Hartford Hospital, Hartford, Conn (Dr Silverman); the {Cerebrovascular Program (Dr Restrepo) and The Johns Hopkins Epilepsy Center (Dr Mathews), Department of Neurology, The Jos Hopkins University School of ‘Medicine, Balimore, Bd: and the Synaptic Physiology Unit, National Institute of [Neurological Disorders and Stroke, ethesda, Md (Dr Mathews). (©2002 American Med 1 Association, All rights reserved. most half (43%) of all patients in the Stroke After Sel- “ares Study experienced a setzure within the first 24 hours alter stroke In a series restricted to early-onset sei- ‘zures, 00% of the 30 patients had ictal activity within the first 24 hours."® Most seizures associated with hemor- rhagie stroke also aceur at onset or within the first 24 hours." During acute ischemic injury, accumulation of in- tracellular caleium and sodium may result in depolar- ization of the transmembrane potential and other ealeiurn- mediated effects. These local ionic shifts may lower the seizure threshold.* Glutamate excitotoxicity is a well- established mechanism of cell death in the experimen- tal stroke model. Antiglutamatergic drugs may also have ‘4 neuroprotective role in ischemic settings, aside from, the role of treating seizures. The size of regional metabolic dysfunction may also bbe relevant in causing early-onset seizures. In the setting ‘of large regions of ischemic hypoxia, high levels of exct- totoxie neurotransmitters may be released extracellu- larly. tn studies of the postischemic brain in experimen- talanimal models, neuronal populations i the neocortex” and hippocampus" have altered membrane properties and increased excitability, which presumably lower the thresh- ‘old for seizure initiation, The ischemic penumbra, a re ‘gion of viable issue adjacent to the infarcted core in is cchemic stroke, contains electrically irritable tissue that may bbe a focus for seizure activity In addition to focal ischemia, global hypoperfusion, ‘can cause seizure activity. Hypoxic-ischemic encepha- lopathy is one of the most common causes of status epi- lepticus and carries a poor prognosis, Particularly vul- nerable to ischemic insult is the hippocampus, which is ‘an especially epileptogenic area In late-onset seizures, by contrast, persistent changes in neuronal excitability occur. Replacement of healthy cell parenchyma by neuroglia and immune cells may play ‘role in maintaining these changes. A gliotic scarring has ‘been implicated as the nidus for late-onset seizures, just 4s the meningocerebral cieatrix may be responsible for late-onset post-traumatic epilepsy ‘An underlying permanent lesion appears to ex- plain the higher frequency of epilepsy in patients with late- than early-onset seizures. Asin post-traumatic epi- lepsy,! late aceurrence ofa first seizure appears to carry «shigher risk for epilepsy. In patients with ischemic stroke, epilepsy developed in 35% of patients with early-onset seizures and in 90% of patients with late-onset sei- ures." The risk for epilepsy was comparable in pa- tients with hemorrhagic stroke; epilepsy developed in 2% of patients with early-onset seizures vs 03% with late The concept that cardiogenic emboli to the brain are more likely to cause seizures acutely iscontroversial, with few supporting data. Among 1640 patients with cere- bral ischemia," events attributed to a cardiae source were most commonly associated with early-onset seizures (26.6%), even compared with supratentorial hemato- mas (162%). However, the definition of cardiogenic mechanisin in this series was often based on nonspe- cific criteria, Several authors have questioned the asso- ciation of seizures with cardioembolic events." Sei- (©2002 American Med zures at onset were not a criterion in a data bank study of the cardiac causes of stroke." Intuitively, there is no reason to suspect that cardigembolie lesions would be more likely than emboli from large-vessel sources to cause seizures, as eardiac and large-vessel emboli frequently in- volve lesions to distal cortical branches. The mecha- nism by which cortical emboli preeipitate seizures is un- certain," but possibilities include depolarization within an ischemic penumbra, rapid reperfusion after the frag- ‘mentation and distal migration ofthe embolus,” ora com bination of both. Cortical location isamong the most reliable risk fae- tors for poststroke seizures. Poststroke seizures were more likely to develop in patients with larger lesions involv- ing multiple lobes ofthe brain than in those with single lobar involvement.® However, any'stroke, including those with only subcortical involvement, may occasionally be associated with seizures» Earlier studies, relying on less sensitive neuroimaging techniques, may not have de- tected concomitant small cortical lesions that could cause ictal activity. The mechanism by which deep hemi- spheric subcortical lesions, most commonly due to small- vessel disease, cause seizures is not understood.” ‘Analogous to cortical involvement in ischemic stroke, a lobar site is considered to be the most epileptogenic lo- cation in patients with intracerebral hemorrhage. Ina se- ries of 123 patients,” seizure incidence was highest with bleeding into lobar cortical structures (54%), low with basal ganglionic hemorrhage (199%), and absent with tha- lamic hemorrhage. Caudate involvement ofthe basal gan- glia and temporal or parietal involvement within the cor- tex predicted seizures.” Hemorthage due to cerebral venous thrombosis also commonly presents with sei- zures. Parenchymal, often cortieal, hemorrhage resull- ing from local venous congestion isthe likely cause of seizure activity The mechanism of seizure initiation by hemorrhage fs not established. Products of blood metabolism, such as hhemosiderin, may eause «focal cerebral irritation leading to seizures, analogous to the animal model of focal epi- lepsy produced by iron deposition on the cerebral cor- tex." In subarachnoid hemorthage, there is often exten- sive hemorrhage into the basal cisterns, which direetly contacts the frontal and temporal lobes. Patients with sub- arachnoid hemorrhage also may have an intraparenchy- ‘mal component to the hemorrhage (Figure 1). The only’ clinical predictor for seizures alter ische- rie stroke isthe severity of the initial neurologic deficit. Greate initial stroke severity” or stroke disability: pre- dicted seizures. By contrast, in the Oxfordshire Commu- nity Stroke Project, only 3% of 225 patients who were in- dependent 1 month after a stroke experienced a seizure between 1 month and 5 years. Patients presenting with greater neurologic impairment tend to have larger strokes that involve wider cortical areas ‘In retrospective studies, risk factors for seizures af- ter subarachnoid hemorthage included middle cerebral artery aneurysms,” intraparenchymal hematoma,” rebralinfaretion,”*a history of hypertension.” and thick- ness of the cisternal clot." By contrast, clinical predic- tors forseizures alter intraparenchymal hemorthage have been lacking. 1 Association, All rights reserved. eae a egal Fare one vay THR r ae [ ChE aban Figure 1. Sevres after intracerebral and sbarachnodhemarthage An 2-ya-od woman presented with sudden-onsat headache, dysphasa and ight hemiparesis hie rcehing antecaglatn thrpy for choi ta filter Computed anograpi (CT) scan at admission A) damonstates an aut et {umporal lobe ntaparenchymal hams, vith adjacent eur a subaachnadhemerroge The respenibl leon, an aneurysm te mid abr ty, was wate sural. During the postopera ped, she ad ep hemisphere. et inde rtrence Vascular lesions may cause seizures by other mechs- nisms. Seizures die to arteriovenous malformations and aneurysms typically occur when these lesions rupture, but these vascular lesions may cause seizures by di- rectly irritating adjacent brain parenchyma (Figure 2) Finally, seizures associated with vascular lesions oc- ‘cur in the setting of significant reperfusion after revasci- larization procedures, most commonly carotid endarter- ‘ectomy for chronic severe extracranial catotid stenosis, The 5 of right-sided facal wing assocated wih anton worsening lhe aphasia (CT scan 3 mri tr (6) showed 2 hypadance sion a the mtrpoal le inthe mil cranial fossa. Ele onataed focal sie waves, consent th seizure act, flawed by focal slowng and proc erazingepepiorm discharge inet capalographi (EEG). reperfusion syndrome, first described by Sundt and col- leagues.” includes transient focal seizure activity, atypical ‘migrainous phenomena, and intracerebral hemorrhage, al- though the clinical triad is often incomplete. Onset ofthis rare syndrome ranges from several days to 3 weeks alter revascularization® and often is signaled by a new ipsila cral headache.” Surgical conection ofan arteriovenous mal- formation may also cause intraoperative oF postoperative hyperemia, with subsequent seizures or hemorrhage." Figure 2. Mass lesion causing oa seizures. 8-yar-old woman presantedt the amargancy department afr fecal anstght-sied loi Imovemens, alowed by lesa consciousness. Computed fmegspic ‘Stan with contrast mans a giant anourysm of the mi cerebral Str wih adjacent coer adaa, corre pt ot the aur, nd Shaan raion whch trom has formed The patent unde ‘ces crantomy. wth thambetemy and aneurysm cing. By contrast, arteriovenous malformations located in border- zone regions subject. relatively low flow rates have a lower risk for hemorrhage.” The reperfusion syndrome has been attributed to im- paired cerebral autoregulation.” In the setting of chronic hypoperfusion due to high-grade carotid stenosis, the ar- terioles responsible for normal autoregulation in the downstream cerebral hemisphere become chronically di- lated. Subsequently, when perfusion is improved by are vascularization procedure, the vessels are incapable of vasoconstriction, and the brain parenchyma is sub- jected to a massive augmentation of blood flow. The re- lease of vasoactive neuropeptides from perivascular sen- sory nerves may contribute to the development of the reperfusion syndrome,” to oxidants that develop before revascularization,” and to an inflammatory response to the reestablishment of circulation.” (CLINICAL MANIFESTATIONS Given that most poststroke seizures are caused by a fo- cal lesion, poststroke seizures are typically focal at on- set. In a study of early-onset seizures in 90 patients, ‘imple partial seizures were the most common type (61%), followed by secondarily generalized seizures (289%). In other series," early-onset seizures were more likely to be partial, whereas late-onset seizures were more likely to generalize secondarily. Most recurrent seizures are of the same type as the presenting episode, and they tend to recur within 1 year on average In a large series of patients with poststroke sei- ‘zures, 9% had status epilepticus.” The only associated, finding was higher functional disability; status epilepti- ‘cus was not associated with higher mortality rate, stroke (©2002 American Medi ype (ischemic or hemorrhagic), topography (cortical in- volvement), lesion size, or eectroencephalographic (EEG) patterns, The phenomenological features of the reperfusion, syndrome are similar in that focal onset with occasional secondary generalization is the rule. Seizure activity always oceurs in the ipsilateral vascular territory of the surgically treated internal carotid artery.® Occasion- ally, status epilepticus ensues (Figure 3) DIAGNOSTIC STUDIES Holmes found that patients with periodic lateralizing epileptiform discharges and bilateral independent pe codkic lateralizing epileptiform discharges on EEG alter stroke were especially prone to the development of sei ures, Those patients with focal spikes also had a high risk of 75%. Focal slowing, diffuse slowing, and normal findings on EEG, by contrast, were associated with rela- Lively low risks of 20%, 10%, and 5%, respectively. Other work found that cortical involvement on results of neuroanatomical imaging studies was more predictive of epilepsy than any single EEG finding," Focal slowing on EEG may simply reflect a wide re- gion of ischemic or infarcted tissue involving the cer bral cortex or subcortical territory. In addition to neu- roimaging, EEG may be helpful in the early evaluation of poorly defined poststroke focal neurologic symp- toms. Inselected patients, focal slowing may confirm the clinical impression of hemispheric ischemia and argue against ongoing seizures as an explanation for an acute neurologic syndrome, The absence of EEG abnormal ies does not definitively exclude cerebral ischemia, par- Uicularly in subcortical or subtentorial structures, oF Uncommon faction on neuroimaging findings. Lansberg etal” recently described several actite magnetic resonance imaging find- {ngs in 3 patients with partial status epilepticus. Thesestud- les showed cortical hyperintensity on diffusion-weighted imaging and T2-weighted sequences and a corresponding, area of low apparent diffusion coefficient. However, these findings were readily differentiated from typical ischemic stroke in their nonvascular distributions, increased signal of the ipsilateral middle cerebral artery on magnetic reso- nance angiography, atid leptomeningeal enhancement on posicontrast magnetic resonance imaging. Another study showed a hyperintensity on dilfusion-weighted images in the dorsolateral portion of the ipsilateral thalamus in 2 patients (Figure 3)."" seizures may mimic ischemia and in- DIFFERENTIAL DIAGNOSIS The differential diagnosis of ischemia-induced seizures in- cludes secondary seizures due to other causes, Medica- tions, drug therapy withdrawal (eg, benzodiazepines), and metabolic disturbances (eg, glucose abnormalities) typi- cally cause generalized seizures, unless an underlying le- sion is already present. Migraine-related focal phenom- ena and transient ischemic attacks may produce focal slowing on EEG findings. Among these entities, glucose abnormalities should not be overlooked 1 Association, All rights reserved. a Facey nero fon J Frm Tr 01 hs mie Ra ar 7 pot rem “ rary, ee k rare) |p ee ' t poe el etn Bet oR BCE Figure 3. Satu eplepicus dt th repartusion syndrome. 65-year-old onan underwent an athervise uncompllatd right cared endartractomy for ‘Seymptomatic extcranl cr artery dace 3 cys cri. She awoke witha headache flan ylet-arm clan movement. These progressed o (zteralaed, tonic-clonic sours, which wor not bora by adrinstaton of loazapam and phonon sodium ray. The contruousslecomeephalograpic {E25} maniar shove perdi stead eploporndschargs occuring every 2b 9 rues, sing ae scores (A). Subsoquant 12- and

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