scholarly journals Psychiatric presentation of voltage-gated potassium channel antibody-associated encephalopathy

2006 ◽  
Vol 189 (2) ◽  
pp. 182-183 ◽  
Author(s):  
U. D. Parthasarathi ◽  
T. Harrower ◽  
M. Tempest ◽  
J. R. Hodges ◽  
C. Walsh ◽  
...  

SummaryVoltage-gated potassium channel antibody encephalopathy, a rare cause of limbic encephalopathy, typically presents with memory impairment and seizures. Psychiatric symptoms have not been emphasised in the literature. Here we describe a 58-year-old man who presented with panic attacks and psychogenic non-epileptic seizures and, later on, developed delusions and hallucinations and then confusion. He was found to have antibodies to voltage-gated potassium channels. Treatment with immuno-modulatory therapy resulted in almost complete recovery.

2020 ◽  
pp. 1-3
Author(s):  
Sena Aksoy ◽  
◽  
Mina Uzülmez ◽  
Aysun Soysal ◽  
◽  
...  

Voltage-gated potassium channel (VGKC) encephalitis is a type of autoimmune encephalitis, that presents with memory impairment, headache, psychiatric symptoms and seizures. Although contactin-associated protein 2 (CASPR2) and leucine-rich glioma inactivated 1 (LGI1) are clearly identifed as components of the VGKC complex, additional subtypes are known to exist. In this report, we present a case of 64-year-old patient with VGKC antibodies, negative for CASPR2 and LGI1


2020 ◽  
Vol 13 (12) ◽  
pp. e233179
Author(s):  
Eric Garrels ◽  
Fawziya Huq ◽  
Gavin McKay

Limbic encephalitis is often reported to present as seizures and impaired cognition with little focus on psychiatric presentations. In this case report, we present a 49-year-old man who initially presented to the Psychiatric Liaison Service with a several month history of confusion with the additional emergence of visual hallucinations and delusions. Due to the inconsistent nature of the symptoms in the context of a major financial stressor, a provisional functional cognitive impairment diagnosis was made. Investigations later revealed a positive titre of voltage-gated potassium channel (VGKC) antibodies, subtype leucine-rich glioma inactivated 1 accounting for his symptoms which dramatically resolved with steroids and immunoglobulins. This case highlighted the need for maintaining broad differential diagnoses in a patient presenting with unusual psychiatric symptoms.


1988 ◽  
Vol 91 (6) ◽  
pp. 817-833 ◽  
Author(s):  
P A Pappone ◽  
M T Lucero

We examined the effects of Pandinus imperator scorpion venom on voltage-gated potassium channels in cultured clonal rat anterior pituitary cells (GH3 cells) using the gigohm-seal voltage-clamp method in the whole-cell configuration. We found that Pandinus venom blocks the voltage-gated potassium channels of GH3 cells in a voltage-dependent and dose-dependent manner. Crude venom in concentrations of 50-500 micrograms/ml produced 50-70% block of potassium currents measured at -20 mV, compared with 25-60% block measured at +50 mV. The venom both decreased the peak potassium current and shifted the voltage dependence of potassium current activation to more positive potentials. Pandinus venom affected potassium channel kinetics by slowing channel opening, speeding deactivation slightly, and increasing inactivation rates. Potassium currents in cells exposed to Pandinus venom did not recover control amplitudes or kinetics even after 20-40 min of washing with venom-free solution. The concentration dependence of crude venom block indicates that the toxins it contains are effective in the nanomolar range of concentrations. The effects of Pandinus venom were mimicked by zinc at concentrations less than or equal to 0.2 mM. Block of potassium current by zinc was voltage dependent and resembled Pandinus venom block, except that block by zinc was rapidly reversible. Since zinc is found in crude Pandinus venom, it could be important in the interaction of the venom with the potassium channel. We conclude that Pandinus venom contains toxins that bind tightly to voltage-dependent potassium channels in GH3 cells. Because of its high affinity for voltage-gated potassium channels and its irreversibility, Pandinus venom may be useful in the isolation, mapping, and characterization of voltage-gated potassium channels.


2008 ◽  
Vol 275 (1-2) ◽  
pp. 185-187 ◽  
Author(s):  
Hirokatsu Takahashi ◽  
Masahiro Mori ◽  
Yukari Sekiguchi ◽  
Sonoko Misawa ◽  
Setsu Sawai ◽  
...  

1993 ◽  
Vol 264 (4) ◽  
pp. C1014-C1019 ◽  
Author(s):  
P. A. Pappone ◽  
S. I. Ortiz-Miranda

Cultured brown fat cells have both voltage- and Ca(2+)-activated potassium channels. We tested whether potassium channel activity is necessary for brown fat proliferation by growing adipocytes and preadipocytes from neonatal rat brown fat in the presence of potassium channel blockers. Whole cell patch-clamp experiments showed that verapamil, nifedipine, and quinine block the voltage-gated potassium current (IK,V) with micromolar affinity. Ca(2+)-activated currents (IK,NE) could be activated by micromolar intracellular Ca2+ concentrations and were blocked by nanomolar concentrations of apamin. Both IK,V and IK,NE are blocked by millimolar concentrations of tetraethylammonium (TEA). Under standard culture conditions, the number of cells showing the multilocular morphology characteristic of brown fat cells doubled in 3-5 days. Continuous exposure to 100 nM norepinephrine had no effect on this process. Cell proliferation was inhibited by TEA, quinine, or verapamil. The inhibition was dose dependent, with concentrations for half-block of cell proliferation similar to the Kd values for block of IK,V. Apamin, which selectively blocks IK,NE, had no effect on cell growth. These results suggest that functional voltage-gated potassium channels, but not Ca(2+)-activated potassium channels, may be necessary for the normal proliferation of brown fat cells in culture.


2016 ◽  
Vol 3 (3) ◽  
pp. 69
Author(s):  
Madhu S Jasti ◽  
Sandipan Pati ◽  
Vinusha Yarlagadda

Faciobrachial dystonic epileptic seizures usually precede the cognitive impairment associated with non-paraneoplastic limbic encephalitis secondary to voltage gated potassium channel complex (VGKC) antibodies, specifically to leucine-rich glioma inactivated 1 (LGI1) antibodies. Testing for VGKC-complex/LGI1 antibodies should be initiated with the recognition of faciobrachial dystonic seizures. This seizure subtype is refractory to treatment with the anti-epileptic drugs, but has been shown to be immunotherapy responsive. Early initiation of immunotherapy has been shown to fasten the time to recovery and also in minimizing the cognitive impairment.


2014 ◽  
Vol 21 (10) ◽  
pp. 1301-1310 ◽  
Author(s):  
B. M. Bettcher ◽  
J. M. Gelfand ◽  
S. R. Irani ◽  
J. Neuhaus ◽  
S. Forner ◽  
...  

Author(s):  
Seyed M. Mirsattari ◽  
Teneille E. Gofton ◽  
Derek J. Chong

Background:Epileptic seizures may be misdiagnosed if they manifest as psychiatric symptoms or seizures occur in patients with known psychiatric illness.Methods:We present clinical profiles of six patients with epilepsy (three male, mean age 39 ± 12 years) that presented with prominent psychiatric symptoms.Results:Two patients had pre-existing psychiatric illnesses. Three patients were initially diagnosed with panic attacks, two with psychosis, and one with schizophrenia. Five patients had temporal lobe epilepsy (TLE) while the sixth patient was subsequently found to have absence status epilepticus (SE). Cranial computed tomogram (CT) including contrast study was unremarkable in five patients and showed post-traumatic changes in one patient. Cranial magnetic resonance imaging (MRI) revealed dysembryoplastic neuroepithelial tumour (DNET) in one patient, cavernous hemangioma in one, and post-traumatic changes plus bilateral mesial temporal sclerosis in another patient but it was normal in two TLE patients. Routine electroencephalography (EEG) revealed absence SE in one patient but it was non-diagnostic in the TLE patients. Video-EEG telemetry in the epilepsy monitoring unit (EMU) was necessary to establish the diagnosis in four TLE patients. None of the patients responded to medications aimed at treating psychiatric symptoms alone. Two patients required surgery while the other four required treatment with anti-epileptic drugs. All the patients had favorable response to the treatment of their epilepsy.Conclusions:This case series illustrates that epileptic patients may experience non-convulsive seizures that might be mistaken as primary psychiatric illnesses. In this subset of patients, evaluation by an epileptologist, MRI of the brain, and/or video-EEG telemetry in an EMU was necessary to confirm the diagnosis of epilepsy if routine EEGs and cranial CT are normal.


2008 ◽  
Vol 39 (01) ◽  
Author(s):  
E Haberlandt ◽  
CG Bien ◽  
A Reiter ◽  
B Simma ◽  
R Crazzolara ◽  
...  

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