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AUTOIMMUNE GABAB ANTIBODY ENCEPHALITIS ASSOCIATED WITH NON–MALIGNANT LUNG LESION
  1. Barbara Wysota,
  2. Lara Teare,
  3. Abid Karim,
  4. Saiju Jacob
  1. University Hospitals Coventry and Warwickshire; University Hospitals of Birmingham

    Abstract

    GABAb receptor autoimmune encephalitis is a potentially treatable disorder characterised by seizures, memory deficits, increased anxiety and mood dysregulation. In some patients it is associated with small–cell lung cancer and with other autoantibodies. We are presenting a case of GABAb receptor autoimmune encephalitis which was associated with non–malignant lung lesion, likely inflammatory in nature.

    A 62 year old woman presented with recent onset depression and tonic–clonic seizures. CT head showed patchy white matter changes particularly in the left frontal lobe. Initial treatment for suspected infective encephalitis with ceftriaxone and acyclovir was withdrawn after normal results of CSF analysis and negative viral PCR. Ongoing seizures were treated with a combination of anticonvulsants. MRI brain showed an encephalitic process involving the temporal lobes (Figure 1) with corresponding change on PET scan. (Figure 2) PET also showed a small nodule in the right lung with a paratracheal lymph node (Figure 3). Diagnosis of paraneoplastic encephalitis secondary to a lung tumour was made during lung MDT. Interval scanning at two months showed an increase in size of the pretracheal lymph node. Testing for VGKC antibodies, anti–TPO, NMDAR antibodies was negative.

    However repeat scan at an interval of six months showed resolution of the chest changes. Patient clinically improved with treatment of the seizures but was left with significant cognitive impairment and epilepsy. Repeat MRI brain one year since symptoms onset showed resolution of the swelling of the medial temporal lobes and hippocampi with atrophy. Signal change was still present. Further antibody testing at this time revealed a raised anti GABAb antibody level.

    GABAb is an inhibitory receptor that has been associated with seizures and memory dysfunction when disrupted. In a recent study 15 patients with encephalitis and GABAb receptor antibodies were clinically assessed. On the basis of clinical, MRI, and EEG findings, the brain regions most affected were the hippocampi and temporal lobes. A third of patients had pathologically confirmed small–cell lung cancer. GABAb receptor autoimmune encephalitis also seems to develop without cancer association. In this respect, GABAb receptor autoimmune encephalitis is similar to other synaptic autoimmune disorders of the CNS.

    After excluding one non–assessable patient, nine of the ten patients who received immunotherapy and cancer treatment (when a tumour was found) showed neurological improvement, while none of the four patients who did not receive immunotherapy or whose tumour treatment was not completed showed improvement.

    Our patient did not receive immunomodulatory therapy as initial investigations were pointing towards paraneoplastic character of encephalitis, which is generally poorly responsive to immunomodulation. GABAb antibodies were tested several months since the onset of patient's symptoms. Patient improved spontaneously but was left with seizures and cognitive deficit as a sequel of her encephalitis.

    GABAb antibody–mediated limbic encephalitis adds to the growing spectrum of autoimmune encephalitides. Seizures are a predominant symptom and initial reports suggests a strong paraneoplastic link, but as more and more patients are described the non–paraneoplastic aetiologies are likely to increase, similar to the other antibodies in this spectrum.

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