LGI1 positive paraneoplastic limbic encephalitis: A case report of atypical presentation

Limbic encephalitis is a rare disorder mainly affecting the medial temporal lobe and is classically paraneoplastic. Autoimmune etiologies also exist, such as antibodies against leucine-rich glioma activated 1 (LGI1). Most cases of anti-LGI1 encephalitis are not associated with tumors. Subacute memory loss is the predominant feature, and most patients develop focal seizures, especially faciobrachial dystonic seizures (FBDSs). Immunotherapies usually show a good response, but are less effective in paraneoplastic cases. We report a case of steroid-responsive anti-LGI1 encephalitis with atypical presentations of sensory aphasia during relapse from rectal carcinoma, an atypical site.

TRANSCORTICAL SENSORY APHASIA AS A MANIFESTATION OF ISCHEMIC STROKE WITH INTRACARDIAC THROMBUS

Transcortical sensory aphasia is characterized by impaired auditory comprehension, with intact repetition and uent speech. A 44-year-old right-handed patient with a history of hypertension on amlodipine and ischemic heart disease on aspirin was admitted to the neurology department for sudden onset of language impairment that started 2 days ago. The patient had features of transcortical sensory aphasia. Brain MRI showed an infarct in the territory of the left middle cerebral artery involving the tempo-parietal region. An apical thrombus was observed in the left ventricle on transthoracic echocardiography. This language impairment is thought to be caused by a disconnection between sensory language processes and semantic knowledge of objects. The prognosis is generally guarded and depends on the etiology and severity of the presentation

Transcortical Sensory Aphasia Sonnet: What Happens When Your Words Are Not Your Own?

A sonnet about transcortical sensory aphasia, a disorder in which comprehension remains intact, but language production is primarily constrained to repetition. Much like the mythical Echo, this sonnet is a reflection upon personal expression when one’s words are not one’s own.

Luxury Perfusion Producing Sensory Aphasia

We describe the case of an 86-year-old Japanese man who, by luxury perfusion after spontaneous recanalization of the left middle cerebral artery/internal carotid artery, produced acute transient sensory aphasia. This rare phenomenon is thought to be caused by reperfusion brain injury.

What are the barriers to participation in a neuromodulation pilot trial for aphasia after stroke?

ABSTRACT Purpose Aphasia is a common and debilitating manifestation of stroke. Transcranial electrical stimulation uses low-intensity electric currents to induce changes in neuronal activity. Recent evidence suggests that noninvasive techniques can be a valuable rehabilitation tool for patients with aphasia. However, it is difficult to recruit patients with aphasia for trials, and the reasons for this are not well understood. This study aimed to elucidate the main difficulties involved in patient’s recruitment and inclusion in a randomized clinical study of neuromodulation in aphasia. Methods We evaluated the reasons for the exclusion of patients in a pilot, randomized, double-blinded clinical trial in which patients diagnosed with motor aphasia after stroke were recruited from March to November 2018. A descriptive statistical analysis was performed. Results Only 12.9% (4) of patients with ischemic stroke were included in the clinical trial. A total of 87.1% (27) of the 31 recruited patients were excluded for various reasons including: sensory aphasia (32.2%), dysarthria (25.8%), spontaneous clinical recovery (16.1%), previous stroke (6.4%), and death or mutism (3.2%). Conclusion The presence of other types of aphasia, dysarthria, spontaneous recovery, deaths, and mutism were barriers to recruiting patients evidenced in this neuromodulation study.

Human Herpesvirus 6 in the CSF of a Woman with New Onset Seizures – Encephalitis or Genomic Integration?

A 55-year-old female was referred to the Neurological Center Rosenhuegel with suspected stroke following sudden-onset sensory aphasia preceded by left-sided intermittent, pulsating ear- and headache, nausea, plus an elementary visual hallucination of bright, flashing, white lights. The ear- and headache began abruptly several days prior to arrival and were responsive to ibuprofen. The hallucinatory symptoms began suddenly after headache onset and lasted approximately five minutes. The patient also experienced aphasia immediately following the hallucinatory symptoms and was promptly transferred to the hospital. She had no known history of chronic illness, including migraines, stroke, seizures, or immunosuppression, and denied having fever or recent illness immediately prior to symptom onset. She had not been taking any regular medications, had not traveled recently, and denied alcohol and substance abuse. Family history was insignificant. Sensory aphasia was noted upon arrival at the hospital. A cranial CT-scan ruled out intracranial hemorrhage and CT-perfusion illustrated hyper-perfusion of the left occipital lobe (Figure 1). As the patient was within the appropriate time frame for thrombolytic therapy, she received intravenous alteplase due to suspected stroke and was asymptomatic the next day.