An initial brain magnetic resonance image “MRI” used Netherlands-manufactured 3-T Philips MR Ingenia Elition (2015) and was unremarkable. tb), Epstein-Barr virus (EBV), Cytomegalovirus (CMV), and enterovirus were all negative. CSF gram stain, culture, cytology, and viral PCRs for HSV I and II, Mycobacterium tuberculosis (M.
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There was no CSF pleocytosis (white blood cell “WBC” count was zero), glucose was normal (3.3 mmol/l, serum glucose 5.3 mmol/l) as well as protein (35 gm/dl). Neurological examination revealed a disoriented and irritable patient with poverty of speech and impaired comprehension, but no focality was discerned throughout the remainder of her limited examination. A review of the medical chart revealed a mostly afebrile patient with two readings of low-grade fever (T. Upon evaluation by neurology, surrogate history was unrevealing of any bulbar symptoms, focal limb weakness, decreased level or loss of consciousness, convulsions, fever, or chills. However, the psychiatry team sensed that the mode and age of presentation were atypical and a warranted exclusion of organic causes. Upon admission, the patient was provisionally diagnosed as a case of acute psychosis and treated accordingly with olanzapine, alprazolam, and thiamine.
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Brain computed tomography (CT) and basic laboratory investigations prior to her referral were reported as free, including a normal thyroid function, normal ESR, and lack of leukocytosis on complete blood count (CBC). Also, a few weeks prior to her symptoms, she suffered from a diarrheal illness that lasted nearly 10 days. Her best friend had recently been diagnosed with terminal lung cancer, and few days before the onset of her symptoms she suffered a severely stressful social encounter. Ī 42-year-old woman who is an active member of society, and who has no previous medical or psychiatric history of note, was referred to the psychiatry department at our tertiary hospital from a peripheral center following a one-week history of an episode marked by progressively disorganized and decreased speech, social withdrawal, labile mood, persecutory delusions, irritability, agitation, decreased sleep, and fluctuating disorientation to place, person, and situation. On the other hand, a normal EEG in some cases may indicate an inorganic disorder. Electroencephalography (EEG) is highly sensitive in encephalitis, especially in chronic cases, but it is rarely specific. Diagnosing encephalitis depends on clinical and radiological evaluation and the findings of CSF analysis, but pinpointing a definite etiology often proves to be more daunting. The clinical presentation is non-specific as patients with encephalitis due to infectious or autoimmune etiologies may present with variable acute or subacute neurologic and/or psychiatric manifestations, with or without fever and cerebrospinal fluid (CSF) pleocytosis. Paraneoplastic encephalitis is usually caused by antibodies against intracellular neuronal proteins, while autoimmune non-paraneoplastic encephalitis in most cases is secondary to antibodies directed against neuronal cell surface or synaptic proteins. Generally, it may be due to infection (such as herpes simplex virus “HSV”) or autoimmunity (paraneoplastic or non-paraneoplastic). Etiologies are diverse, and the differential diagnosis of encephalitis is often complex. We encourage practicing physicians to use EEG as an early, sensitive diagnostic tool for cases suspected to have autoimmune encephalitis.Įncephalitis is a serious condition with the potential to cause severe and permanent disability or even death. The recently introduced diagnostic criteria for autoimmune encephalitis included new-onset seizures in the earliest steps in the algorithm but did not yet incorporate EEG findings. DiscussionĮEG is highly sensitive and rarely normal in encephalitis. We describe the case of a 42-year-old woman who did not initially meet the newly proposed criteria for probable autoimmune encephalitis, but in whom the detection on electroencephalogram (EEG) of subtle asymmetric slowing of the left hemisphere ultimately led to the diagnosis. Collectively, these factors predispose for delays in diagnosis and treatment in many cases. Finally, the different diagnostic approaches lack consensus and have until recently been largely retrospective. Laboratory testing for pathogenic neuronal antibodies is limited by accessibility and sensitivity issues. In many cases, MRI and CSF studies return normal. Autoimmune encephalitis presents with subacute neurological, psychiatric, and behavioral symptoms.