Aphasic Status Research Articles

Nonconvulsive status epilepticus in patients with acute subarachnoid hemorrhage is associated with negative arterial spin labeling on peri-ictal magnetic resonance images

PurposeNon-convulsive status epilepticus (NCSE) is characterized by repetitive or continuous seizures without convulsions. Arterial spin labeling (ASL) is useful for assessing hyperperfusion due to neurovascular unit coupling in patients with NCSE; subarachnoid hemorrhage (SAH) impairs the neurovascular unit. We hypothesized that the sensitivity of ASL in detecting NCSE is low in patients with SAH during the acute phase. MethodsBased on ASL findings obtained within 48 h after the clinical suspicion of focal-onset NCSE, we divided 34 patients into ASL-negative (no hyperperfusion; n = 10) and ASL-positive (confirmed hyperperfusion; n = 24) groups. We further divided the two groups according to the NCSE etiology: patients who were diagnosed with NCSE within 14 days after SAH onset (acute SAH, n = 11) and patients with NCSE due to factors other acute SAH (n = 23) and compared their characteristics. ResultsIn 10 of the 34 patients (29.4 %) the ASL findings were normal. The rate of acute SAH was significantly higher in ASL-negative- (n = 8, 80.0 %) than ASL-positive patients (n = 3, 12.5 %). The rate of patients in aphasic status was significantly lower in ASL-negative patients (n = 1, 10 %) than in ASL-positive patients (n = 12, 50.0 %). ConclusionNormal ASL findings alone should not be used to exclude a diagnosis of NCSE particularly in patients in the acute phase of SAH with deterioration or no improvement in consciousness.

Isolated aphasic status epilepticus: CT perfusion, SPECT and EEG reveal neurovascular coupling and support the differential diagnosis.

Objective Among the clinical manifestations of stroke mimics, isolated aphasia is one of the most challenging due to its aetiopathogenic diagnosis. This short communication describes a specific perfusion and brain oscillatory pattern in a challenging case of prolonged isolated aphasia caused by status epilepticus, jointly investigated by computed tomography (CT) perfusion, single-photon emission computerized tomography (SPECT)/CT and EEG qualitative and quantitative analysis. Methods We discuss the different patterns of perfusion neuroimaging and EEG between SE and ischaemic stroke or postictal (Todd's)-related isolated aphasia, and propose these differences as a basis to support the differential diagnosis. Results The pattern associated with SE was characterized by focal hyperperfusion on CT perfusion maps (the left mean transit time was shorter with >10% asymmetry, and left cerebral blood volume and cerebral blood flow increased or slightly altered, relative to the contralateral side) and SPECT (focal left temporal hyperperfusion), without any early ischaemic signs on non-enhanced CT, while the EEG showed a predominant left hemispheric slow delta power. The aforementioned perfusion pattern contrasts with postictal epileptic Todd's phenomenon, which is characterized by hypoperfusion on CT perfusion (the mean transit time is prolonged and cerebral blood volume and cerebral blood flow are reduced, compared to the contralateral hemisphere) and SPECT (focal hypoperfusion), not restricted to the specific vascular territories. Significance CT perfusion patterns may add valuable information to support the differential diagnosis of status epilepticus, rather than acute ischaemic stroke or postictal Todd's phenomenon, in cases with challenging symptoms of prolonged isolated aphasia.

Cytotoxic lesion of the corpus callosum in a patient with aphasic status epilepticus

A 47-year-old man with a history of aphasic seizures presented to the emergency room with a 12-hour global aphasia. Upon admission, brain MRI did not reveal acute lesions, and EEG showed sharp waves in the left frontal-temporal region. An Aphasic Status Epilepticus was diagnosed and antiepileptic treatment was initiated with adequate response. A week after the episode, a new brain MRI showed a high-signal ovoid lesion on T2-weighted and FLAIR sequences in the central part of the splenium of the corpus callosum. On diffusion-weighted images (DWI) the lesion was hyperintense with decreased apparent diffusion coefficient (ADC) values, indicating restricted diffusion consistent with a cytotoxic lesion of the corpus callosum (CLOCC). Follow-up MRI one month later showed complete image resolution. CLOCCs are secondary lesions associated with various entities in which high levels of cytokines and extracellular glutamate cause intracellular edema and reduced diffusion, a condition called cytotoxic edema, which affects vulnerable brain regions such as the splenium of the corpus callosum. In epileptic patients, CLOCCs may be due to the effect of seizures, especially prolonged ones, as well as antiepileptic treatment itself. CLOCCs are rare radiological findings and must be recognized to avoid misdiagnosis.

Cytotoxic lesion of the corpus callosum in a patient with aphasic status epilepticus

A 47-year-old man with a history of aphasic seizures presented to the emergency room with a 12-hour global aphasia. Upon admission, brain MRI did not reveal acute lesions, and EEG showed sharp waves in the left frontal-temporal region. An Aphasic Status Epilepticus was diagnosed and antiepileptic treatment was initiated with adequate response. A week after the episode, a new brain MRI showed a high-signal ovoid lesion on T2-weighted and FLAIR sequences in the central part of the splenium of the corpus callosum. On diffusion-weighted images (DWI) the lesion was hyperintense with decreased apparent diffusion coefficient (ADC) values, indicating restricted diffusion consistent with a cytotoxic lesion of the corpus callosum (CLOCC). Follow-up MRI one month later showed complete image resolution. CLOCCs are secondary lesions associated with various entities in which high levels of cytokines and extracellular glutamate cause intracellular edema and reduced diffusion, a condition called cytotoxic edema, which affects vulnerable brain regions such as the splenium of the corpus callosum. In epileptic patients, CLOCCs may be due to the effect of seizures, especially prolonged ones, as well as antiepileptic treatment itself. CLOCCs are rare radiological findings and must be recognized to avoid misdiagnosis.

Junctional bradycardia caused by subarachnoid hemorrhage

The electrocardiogram in subarachnoid hemorrhage patient is in many ways. A 69-year-old female felt headache and then collapsed an hour prior to arrival of emergency room. Her vital signs were a body temperature of 37 °C, heart rate of 51 beats per minute, and blood pressure of 224/135 mm Hg. Physical examinations revealed comatose with Glasgow Coma Scale E1V1M1 and fast glucose level test showed 238 mg/dl. Initial electrocardiogram (ECG) revealed junctional bradycardia (51 beats per minute) with T inversion over lead V2 to V6. Cranial computed tomography (CT) scan was performed and revealed diffuse subarachnoid hemorrhage (SAH) in the subarachnoid cisterns, bilateral sylvian fissures, left frontal sulci, left temporal cortical sulci, and interhemispheric fissure as well as lateral, third and fourth ventricles. External ventricular drainage was placed by neurosurgeon and patient was then admitted to intensive care unit. She was discharged with a bedridden and aphasic status 32 days later. Repolarization abnormalities, such as ST-segment change, T wave inversion and QTc prolongation, are also commonly seen in ECGs of patients with SAH. Physicians should keep in mind of junctional bradycardia not certainly as a cardiac problem, it may appear in cranial emergency.

Aphasic status epilepticus in a tertiary referral center in Turkey: Clinical features, etiology, and outcome

ObjectiveAphasic status epilepticus (ASE), although rare, may often remain underdiagnosed. We aimed to report the patients diagnosed with ASE and describe their clinical presentation, etiology, electrophysiological findings, neuroimaging, treatment options, and outcome. MethodsWe retrospectively analyzed a series of 28 patients diagnosed with ASE between January 2010 and August 2019 in our tertiary referral center. We reviewed medical files, patient charts, and short- and long-term intermittent electroencephalogram (EEG) recordings. Demographical, historical, clinical, neuroimaging, electrophysiological parameters, administered antiseizure medications, and prognosis of all patients were recorded. Furthermore, EEGs were re-evaluated according to Salzburg criteria. ResultsMost patients presented with tumors (n = 11) and cerebrovascular disease (CVD) (n = 11), while the rest were diagnosed with hyperglycemia (n = 2), autoimmune encephalitis (n = 1), remote intracranial abscess (n = 1), mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) attack (n = 1), or unknown cause (n = 1). Seventy-one percent of patients had prior history of epilepsy. The most common EEG findings were rhythmic delta activity with fluctuation and epileptiform discharges ≤ 2.5 Hz with spatiotemporal evolution (66 %). Magnetic resonance imaging (MRI) and EEG findings indicated dominant hemisphere involvement in all patients. No casualties occurred; 71 % patients exhibited total recovery, while 29 % had mild-moderate sequela aphasia. None of the patients received aggressive treatment for ASE. SignificanceA relatively higher number of ASE patients could be contributed to the literature through this study. ASE should be considered in patients with prolonged unexplained aphasia, especially with pre-existing risk factors, such as prior history of epilepsy, structural lesion, and metabolic disorders accompanied by concordant EEG findings. Although the underlying cause is a determining prognostic factor, this study shows a significant number of patients with complete remission; thus, the prognosis of ASE may be considered more favorable than other types of nonconvulsive status epilepticus.

Lateralized Periodic Discharges (LPDs) as ictal manifestation of Aphasic Status Epilepticus

Lateralized Periodic Discharges (LPDs) as ictal manifestation of Aphasic Status Epilepticus

When aphasia is due to aphasic status epilepticus: a diagnostic challenge.

Aphasic status epilepticus is an uncommon entity that should be included in the differential diagnosis of persistent and sudden language disorders. In our study, we describe seven patients admitted with clinical and electroencephalographic diagnosis of aphasic status, who were studied with both neuroimaging and electroencephalogram. The mean age was 65.9years (range of 39-89). Three of the patients had previously been diagnosed of epilepsy. The aphasia was global in six patients. In one case, we found foci of the left hemorrhagic contusions. The initial electroencephalogram (EEG) was not conclusive of status in two patients. In one patient, neuroimaging showed left hemispheric hypoperfusion, compatible with postictal changes. Six out of seven patients required at least two antiepileptic drugs. Three patients died of systemic complications (infectious causes), whereas the other four cases had a complete recovery. Our study highlights that a second EEG study might be necessary to confirm epileptiform activity, when clinical features and other tests suggest an epileptic origin. An early and specific treatment, avoiding or diminishing comorbidities, might significantly improve the prognosis of these patients.

Aphasic status epilepticus as the sole symptom of epilepsy: A case report and literature review.

Aphasia is a common symptom encountered by neurologists. However, the presence of aphasia as the sole manifestation of partial status epilepticus is rare. The present study reports a case of aphasic status epilepticus in a 27-year-old right-handed female who presented after the abrupt onset of aphasia, which had persisted for 1.5 days. The patient's medical history included head trauma followed by a craniectomy and cranioplasty. Computed tomography scans revealed a lesion in the patient's left parietal lobe, and an electroencephalogram showed a spike and slow wave pattern in the left hemisphere of the brain during aphasia. The patient's condition improved after the oral administration of oxcarbazepine daily. In the present study it was observed that EEGs were a simple method to diagnose aphasic seizures and therefore EEG recordings should be performed in all cases of unexplained aphasia. In addition, the present study reviewed previously reported cases of aphasic status epilepticus.

Isolated Aphasic Status Epilepticus as a Manifestation Induced by Hyperglycemia Without Ketosis

Diagnosis of aphasic status epilepticus (ASE) is very difficult, because the literature containing, to our knowledge, isolated non-ketotic hyperglycemia (NKH)-related ASE has reported only three cases. Although most cases are associated with organic brain lesions accompanying other clinical seizure activity, NKH-related ASE is rarer. We describe a rare case of NKH presenting initially as persistent and isolated ASE. Brain magnetic resonance imaging (MRI) did not reveal any focal lesion, but ictal electroencephalography (EEG) disclosed diffuse continuous theta to delta waves, intermingled with epileptiform discharges. Only correcting the hyperglycemia could not improve the language disorder completely, and the seizure was controlled only by the addition of phenytoin immediately. Patients with NKH may initially present with isolated ASE. Unlike stroke-related aphasia, accurate diagnosis is difficult if based solely on neurologic examination and brain neuroimaging. Use of EEG and blood sugar determination should be helpful in this special case. Prompt treatment including correcting the hyperglycemia would substantially improve the outcomes of NKH but might be insufficient. Additional prompt use of antiepileptic drugs might be potentially more effective. J Neurol Res. 2016;6(4):85-88 doi: http://dx.doi.org/10.14740/jnr395w

Isolated Aphasic Status Epilepticus as a Manifestation Induced by Hyperglycemia Without Ketosis

Diagnosis of aphasic status epilepticus (ASE) is very difficult, because the literature containing, to our knowledge, isolated non-ketotic hyperglycemia (NKH)-related ASE has reported only three cases. Although most cases are associated with organic brain lesions accompanying other clinical seizure activity, NKH-related ASE is rarer. We describe a rare case of NKH presenting initially as persistent and isolated ASE. Brain magnetic resonance imaging (MRI) did not reveal any focal lesion, but ictal electroencephalography (EEG) disclosed diffuse continuous theta to delta waves, intermingled with epileptiform discharges. Only correcting the hyperglycemia could not improve the language disorder completely, and the seizure was controlled only by the addition of phenytoin immediately. Patients with NKH may initially present with isolated ASE. Unlike stroke-related aphasia, accurate diagnosis is difficult if based solely on neurologic examination and brain neuroimaging. Use of EEG and blood sugar determination should be helpful in this special case. Prompt treatment including correcting the hyperglycemia would substantially improve the outcomes of NKH but might be insufficient. Additional prompt use of antiepileptic drugs might be potentially more effective. J Neurol Res. 2016;6(4):85-88 doi: http://dx.doi.org/10.14740/jnr395w

A Case of Isolated and Prolonged Global Aphasia: Ischemic Stroke or Aphasic Status Epilepticus?

Introduction: The most common cause of sudden isolated and prolonged global aphasia is acute stroke, affecting the cortical or subcortical language network. However, an aphasic status epilepticus (ASE) has to be considered as a possible differential diagnosis in awake patients presenting with acute and prolonged language impairment. ASE is suggestive of a localized dysfunction of language processing in the dominant hemisphere. ASE is a rare phenomenon and few cases are reported in the current literature. In the differential diagnosis between ASE and stroke with aphasia, FDG-PET imaging could be used when EEG shows no clear evidence of epileptic activity. Case Presentation: We described a case of a 74 year-old woman who presented sudden

Isolated Aphasic Status Epilepticus as Initial Presentation of Nonketotic Hyperglycemia

Diagnosis of aphasic status epilepticus is sometimes not easy because of its rarity and electroclinical dissociation. Although most cases are associated with organic brain lesions, nonketotic hyperglycemia (NKH)-related aphasic status epilepticus is rare, especially if it is isolated (without other clinical seizure activity). On the other hand, unlike other metabolic disorders, or hypoglycemia-related generalized seizures, focal motor seizure and epilepsia partialis continua can occur in 25% of NKH, with seizures being the initial manifestation in up to 50% of patients. However, the presentation of epileptic aphasia is rare in NKH patients. We report a rare case of NKH presenting initially as persistent and isolated aphasic status epilepticus. Brain magnetic resonance imaging did not reveal any focal lesion, but ictal electroencephalography (EEG) disclosed left frontotemporal continuous theta to delta waves, intermingled with epileptiform discharges. Correcting the hyperglycemia failed to improve the language disorder, and the seizure was controlled only by the addition of carbamazepine. Patients with NKH may initially present with isolated aphasic status epilepticus. Unlike stroke-related aphasia, accurate diagnosis is difficult if based solely on neurologic examination and brain neuroimaging. Use of EEG and blood sugar determination should be helpful in this special condition.

Early Appearance of Diffusion-Weighted Hyperintensities in Aphasic Status Epilepticus

Partial status epilepticus rarely manifests mainly with global aphasia. It usually results in diffusion-weighted imaging (DWI) abnormalities after prolonged seizures. We discuss the magnetic resonance imaging (MRI) findings in a patient with aphasic status epilepticus. MRI showed diffusion restriction four hours after onset of symptoms. We summarize previously reported brain imaging findings in status epilepticus and discuss the purported mechanism behind these changes. Findings in our patient, similar to few others described in the literature, suggest that cortical DWI hyperintensities can occur shortly following aphasic status epilepticus.

Aphasic status epilepticus: Electroclinical correlation

Aphasic status epilepticus (ASE) in otherwise awake patients is a rare phenomenon. We present a series of nine consecutive patients with ASE to characterize clinical, electrophysiologic, and imaging findings. Nine patients in ASE were identified between July 2006 and December 2009 at our institution. Each was evaluated by the neurology service and monitored with video-electroencephalography (EEG) for at least 24 h. Thorough, repeated language testing was correlated with EEG findings. All nine patients were right-handed with subacute or chronic left hemispheric lesions on magnetic resonance imaging (MRI). All patients had mixed aphasia, three presenting with persistent aphasia from onset and six with episodic speech impairment, which became persistent in five of the six. The initial 30-min EEG demonstrated electrographic seizure in only five patients (56%), despite the presence of aphasia during the recording. Left hemispheric periodic lateralized epileptiform discharges (PLEDS) were seen in two patients, and left hemispheric slowing in two patients. Continuous video-EEG monitoring confirmed electrographic seizure activity in all nine patients. Peak electrographic seizure frequency varied from continuous to once every 2 h and was not associated with fluctuations in the speech deficit. EEG seizures resolved abruptly in three patients and gradually over up to 4 days in six patients. Clinical improvement was delayed in eight of the nine patients, and four patients retained some aphasia at discharge, 2-4 days after EEG seizure resolution. Standard EEG is sensitive for detection of abnormalities in the dominant hemisphere in patients with ASE. However, continuous EEG is necessary to confirm the diagnosis and monitor treatment, since clinical symptoms do not correlate with electrographic seizure activity and do not provide sufficient information to guide treatment decisions.

Recurrent aphasic status epilepticus after prolonged generalized tonic–clonic seizures versus a special feature of Todd's paralysis

Postictal aphasia may be a feature of Todd's paralysis or the presentation of aphasic nonconvulsive status epilepticus (NCSE). We describe a 74-year-old woman with three episodes of aphasic status epilepticus after prolonged generalized tonic–clonic seizures. In the first episode, the NCSE was not definitively diagnosed, but an increase in the epileptic medication led to resolution of the epileptic activity within 2weeks. During the second episode, NCSE was terminated within 7days under intensified antiepileptic treatment. In the third episode, phenytoin treatment led to intoxication and resulted in further treatment on an intensive care unit. The patient required several months to recover from this episode. NCSE in the elderly is difficult to recognize, especially when it presents as a prolonged postictal deficit like aphasia. Once diagnosed it has to be treated carefully, because in the elderly, aggressive treatment strategies may be associated with a high risk of adverse events.

Aphasic or amnesic status epilepticus detected on PET but not EEG

To describe five patients with ictal aphasia and one patient with ictal amnesia, who had focal positron emission tomography (PET) hypermetabolism but no clear ictal activity on electroencephalography (EEG). (18)F-Fluorodeoxyglucose (FDG)-PET scans with concomitant EEG were obtained in five patients with suspected ictal aphasia or ictal amnesia without ictal activity on EEG. We reviewed medical history, EEG, imaging data, and treatment outcome. Brain magnetic resonance imaging (MRI) showed no structural abnormalities in any of the patients. EEG showed left temporal irregular delta activity in three patients, with aphasia and nonspecific abnormalities in two other patients, all without clear ictal pattern. All patients demonstrated focal hypermetabolism on PET scan. The hypermetabolism was in the left frontotemporal region in patients with ictal aphasia and in the bilateral hippocampal region in the patient with amnesia. Three patients who received intravenous benzodiazepines during their episodes had transient clinical improvement. With antiepileptic drug (AED) treatment, symptoms gradually resolved in all patients. Concomitant resolution of PET hypermetabolism was documented in three patients who had follow up scans. One patient with ictal aphasia later developed recurrent episodes, each with recurrent PET hypermetabolism. This patient and one other patient required immune-modulating therapy in addition to AEDs. FDG-PET imaging should be considered as a diagnostic tool in patients with suspected ictal aphasia or amnesia, who fail to show clear evidence of ictal activity on EEG.

MRI findings in aphasic status epilepticus

Ictal-MRI studies including diffusion-weighted imaging (DWI), perfusion-weighted imaging (PWI), and MR-angiography (MRA) in patients with aphasic status epilepticus (ASE) are lacking. In this report, we aim to describe the consequences of the ASE on DWIs and its impact on cerebral circulation. We retrospectively studied eight patients with ASE confirmed by ictal-EEG, who underwent ictal-MRI shortly after well-documented onset (mean time delay 3 h). ASE consisted in fluctuating aphasia, mostly associated with other subtle contralateral neurological signs such as hemiparesia, hemianopia, or slight clonic jerks. In MRI, six patients showed cortical temporoparietal hyperintensity in DWI and four of them had also ipsilateral pulvinar lesions. Five patients showed close spatial hyperperfusion areas matching the DWI lesions and an enhanced blow flow in the middle cerebral artery. Parenchymal lesions and hemodynamic abnormalities were not associated with seizure duration or severity in any case. The resolution of DWI lesions at follow-up MRI depended on the length of the MRIs interval. In patients with ASE, lesions on DWI in the temporo-parietal cortex and pulvinar nucleus combined with local hyperperfusion can be observed, even when they appear distant from the epileptic focus or the language areas.

Aphasic status epilepticus with periodic lateralized epileptiform discharges in a bilingual patient as a presenting sign of “AIDS–toxoplasmosis complex”

We describe an HIV-infected, bilingual patient presenting with Wernicke’s aphasia due to partial status epilepticus with periodic lateralized epileptiform discharges, as the first sign of AIDS–toxoplasmosis complex. The localization of the native and secondary language centers in the brain and the possible role of recurrent seizures in the fluctuating course of Wernicke’s aphasia in this patient are discussed. The clinical course of this patient supports the belief that a second language area for a second language learned in the later stages of life is located in an area different from that for the native language but still in close proximity to it.

Nonconvulsive status epilepticus presenting as a subacute progressive aphasia

We report a 62-year-old man with non-convulsive status epilepticus (NCSE) presenting as a progressive aphasia that developed insidiously over 5 weeks. On video-EEG monitoring, aggravation of the aphasia coincided with occurrence of seizure activities arising from the left fronto-temporal area. Brain MRI was noncontributory but a fluorodeoxyglucose-PET scan revealed a hypometabolism in the left anterior temporal area. Following anticonvulsant treatment, aphasia recovered gradually over several weeks despite prompt resolution of epileptic discharges on EEG. Our patient’s findings, gradual onset of isolated aphasia with gradual resolution after initiation of treatment, may differ from previously reported cases with aphasic status epilepticus because their aphasia showed abrupt onset and rapid resolution with anticonvulsant medication.