Impact of poststroke seizures on neurological deficits: magnetic resonance diffusion-weighted imaging study.

BACKGROUND: The impact of poststroke seizures on the neurological deficits related to ischemic stroke is not well known. It has been reported that following poststroke epilepsy, transient or long-lasting worsening of the poststroke sequelae may develop, but the underlying mechanism of deficit worsening has not been systematically studied by magnetic resonance diffusion-weighted imaging (MRI-DWI). METHODS: From 2008 to 2009, 1,010 ischemic stroke patients were admitted to our stroke unit at the Ege University Hospital with first-time strokes. Of these, 76 (7.5%) patients developed delayed seizures in a follow-up period of 18 months. We extracted the clinical and imaging data of the patients from our Stroke Registry databases and other medical records, and evaluated brain MRI, including spin-echo DWI with apparent diffusion coefficient (ADC) maps, FLAIR and T2-weighted images. RESULTS: There were 15 (20%) patients who had long-lasting worsening of the previous neurological sequelae, which we called long-lasting neurological worsening (LLW); 38 (50%) had transient neurological worsening (TNW) and 23 (30%) were without neurological worsening (WNW) after poststroke seizures. DWI findings were present in 3/23 (13%) patients with simple partial-type seizure, in 4/17 (29%) patients with complex partial-type seizure, and in 7/13 (54%) patients with generalized toni-clonic type seizure (p = 0.002). Patients with LLW showed more frequent changes on DWI than those with TNW (53 vs. 16%; p = 0.009). Forty percent of patients with LLW and 5% of those with TNW had ADC decrease (p = 0.004). Patients with LLW had DWI changes in the occipital region more frequently than those with TNW (57 vs. 18%; p = 0.05). Correlation analysis found a significant association between LLW and DWI changes, multiple DWI lesions, ADC decrease, and recurrent seizures. In the control MRI-DWI 1 month after the poststroke seizure, no signal abnormalities were detected in neuroimaging studies of all patients. Despite no functional outcome differences between the groups before the seizure, the functional scales 1 week after the seizure (National Institutes of Health Stroke Scale, Modified Rankin Scale and Barthel Index) showed significantly worse neurological functional statements in the patients with LLW than those with TNW and WNW (p = 0.001). CONCLUSIONS: Poststroke seizures may affect poststroke sequelae transiently, which we see more often, but some seizure types may prolong the duration of deficits. Multiple DWI changes and LLW following recurrent and longer poststroke seizures were strongly associated, and this may be due to the effect of seizures causing additional metabolical changes.

Charles Bonnet Syndrome in a Patient With Right Medial Occipital Lobe Infarction: Epileptic or Deafferentation Phenomenon?

BACKGROUND: Charles Bonnet syndrome (CBS) is an uncommon disorder characterized by complex and recurrent visual hallucinations in patients with visual pathway pathologic defects. OBJECTIVE: To describe a patient who experienced complex visual hallucinations following infarction in the right occipital lobe and epileptic seizure who was diagnosed as having CBS. PATIENT: A 65-year-old man presented acute ischemic stroke caused by artery to artery embolism involving the right occipital lobe. RESULTS: Following ischemic stroke, complex visual hallucinations in the left visual field not associated with loss of consciousness or delusion developed in the patient. Hallucinations persisted for >1 month and during hallucination, no electrographic seizures were recorded through 24 hours of videoelectroencephalographic monitoring. CONCLUSIONS: CBS may develop in a patient with occipital lobe infarction following an embolic event. CBS associated with medial occipital lobe infarction and epilepsy may coexist and reflects the abnormal functioning of an integrated neuronal network.

[Epidural blood patch treatment in a patient with chronic headache related to spontaneous intracranial hypotension]. / Spontan intrakraniyal hipotansiyona bagli kronik bas agrisi olan hastada epidural kan yamasi tedavisi.

Intracranial hypotension is usually seen in middle-aged adults and appears with orthostatic headache. It is characterized by low cerebrospinal fluid (CSF) pressure and pachymeningeal-dural thickening on magnetic resonance imaging (MRI). Lumbar puncture, dural rupture with CSF leakage secondary to spinal anesthesia or spinal traumas, and under-production or over-absorption of CSF due to some metabolic events such as dehydration, uremia and diabetic coma are the main etiologic factors. It is sometimes considered as idiopathic when no etiologic factor is present. In addition, some connective tissue disorders have risk of CSF leakage due to spontaneous dural rupture. Neck pain, tinnitus, nausea and vomiting, and diplopia may accompany headache. CSF leakage can be identified by computerized tomography (CT) myelography, CSF-flow MRI, and radionuclide cisternography. Bed rest, fluid resuscitation, caffeine, theophylline, and non-steroidal antiinflammatory drugs (NSAIDs) are important treatment options. In patients resistant to therapy, interventional measures such as epidural saline or blood patch can be applied. In this case report, we evaluated the results of pain treatment options in a patient having headache due to intracranial hypotension who was hospitalized in the Neurology Department of Ege University Hospital.