Chest Pain, Hemoptysis, and Loss of Consciousness Masquerading Autoimmune Encephalitis
Year: 2025
Type: article
Abstract: Dear Editor, A 38-year-old man, with no previous medical history, presented with recurrent episodes of severe chest pain followed by loss of consciousness lasting five minutes over the past 2 months. There was no involuntary movement, but blood trickled down the mouth during the attack(s) without any visible injury (hemoptysis was suspected in view of fresh blood leak without any tongue bite). His cardiac workup, which included cardiac enzymes, Pro-B-type Natriuretic Peptide, transesophageal echocardiogram, coronary angiogram, and prolonged cardiac monitoring, was normal. A Computed Tomography (CT) scan of the chest, pulmonary angiogram, bronchoscopy, upper gastrointestinal endoscopy, and Magnetic resonance imaging (MRI) of the brain revealed no significant findings. Levetiracetam followed by sodium valproate was added when he continued to have attacks with the first antiepileptic drug. However, as the frequency of attacks escalated, our institute admitted him. His clinical examination was unremarkable during the initial presentation, but his sensorium subsequently deteriorated and he became drowsy. Though during the initial presentation with normal sensorium, the interictal Electroencephalogram (EEG) was normal, subsequently generalized epileptiform discharges were noted in the background of an encephalopathic pattern. All other tests, including routine blood tests, tests for vasculitis, metabolic parameters (electrolytes, renal function, liver function tests, ammonia, thyroid profile, anti-Thyroid Peroxidase antibody, anti-Thyroglobulin antibody), markers of infection were within normal limits. The detailed studies of cerebrospinal fluid which included routine, paired CSF, and serum autoimmune panels (anti NMDA, anti CASPR2, anti LG1, anti AMPA2, GABA receptor antibodies), paraneoplastic markers, infectious panels, tests for CSF IgG index, and oligoclonal band were all unremarkable. 18F-fluorodeoxyglucose-positron emission tomography (FDG PET CT) scan of the whole body was conducted, diffuse hypermetabolism in both medial temporal cortices, both basal ganglia, and thalami were noted and possibility of seronegative autoimmune encephalitis was considered [Figure 1]. We started him on intravenous immunoglobulin and steroids (concluding seronegative autoimmune encephalitis as the likely possibility with unique areas of hypo and hypermetabolism in PET CT scan of the brain and he showed remarkable improvement). Over the next few days his sensorium improved and EEG showed normal wave pattern. While PET CT scans in autoimmune encephalitis classically reveal hypermetabolism in the medial temporal lobes (hippocampus and amygdala), basal ganglia, and sometimes the frontal lobes, our patient revealed diffuse hypermetabolism not only in both medial temporal cortices and basal ganglia but also in thalami.Figure 1: FDG PET CT scan of the brain showing diffuse hypermetabolism in both medial temporal cortices, basal ganglia, and thalami with hypometabolism in both cerebellar lobes in (a) Coronal view, (b) Axial viewOur case presents three intriguing points. Firstly, epileptic seizures can reduce the stability of the blood-gas barrier and increase the permeability of the pulmonary vascular system resulting in neurogenic pulmonary edema which could lead to hemoptysis.[1] This mechanism has been reported as a cause of sudden unexpected death in epilepsy in patients with generalized tonic-clonic seizures. However, our patient did not have convulsions. Secondly, after ruling out common causes of chest pain, we must consider the possibility that the brain could be the origin of the pain. Some parts of the brain that may be involved in chest pain are the inferior frontal lobe, the right anterior insula especially on the right side, the mesial parietal lobe, the cingulate cortex, the hypothalamus, periaqueductal gray matter, thalami, and the prefrontal cortex.[2] Finally, FDG PET CT is more sensitive (almost 85%) in autoimmune encephalitis compared to MRI (40%), CSF (62%), and EEG (30%).[3] When our suspicion for an autoimmune etiology is high, we should maintain a low threshold for performing the test for early detection and intervention of the disease, as delay may lead to catastrophic consequences. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
Source: Neurology India
Authors: Debabrata Chakraborty, Manoj Kumar Mahata, Nabarun Roy, Arindam Mukherjee
Language: English
Subfield: Clinical Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
OpenAlex ID: W4409499334