PANSS SCORE & LATEST UPDATE

It is Elizabeth’s Birthday on Monday. She is 37, her life and mine ruined by NHS/social services.  Police on the other hand have not acted unprofessionally towards us. All we have encountered under the NHS has dishonesty, bullying and cruelty. There is no sign whatsoever of the Oliver McGowan training. has been no decent communication towards us as a family. To deprive leave is cruelty. To take away every bit of enjoyment by locking away her mobile phone is cruelty. To pick on and bully a mother like me is nasty. I have been banned for months on end from visiting and am told I cannot visit the ward alone.  In any case I do not feel safe to step foot alone in that place any more as they have called the Police out so many times are reporting adversely- writing notes during visits and God knows what is being said behind our backs. This is all aimed at me because I have dared to challenge but everyone goes along with what they are being instructed. It is not out of concern for the patient it is brutal bullying – that is what we or rather I have encountered. I have requested records under Data Protection only for my requests to be ignored and I have had to go to the ICO. There are no doubt awful things written behind my back and to call Police on so many occasions which makes you wonder what is being reported against you.  Do they not even stop to think Police are busy and they are wasting Police time rather than try to make out they have cause to ask them to visit the ward.  This is being done to threaten and bully me and deter me from making contact whilst they continue to hold my daughter a prisoner indefinitely. It is not done out of concern or kindness for the vulnerable patient who is suffering. The reason is I do not trust anyone working for LINOLNSHIRE PARTNERSHIP TRUST is that they are using the point that it is no individual person’s responsibility and that all the professionals agree with their actions which most certainly go against their code of conducts.  My whole point is that the agencies assigned to protect seem to be doing nothing.

CQC have visited ward - then you get a letter and they do not want to get involved. The PHSO, LG Ombudsmen are other examples who dismiss a complaint they know full well they cannot defend. The defence is not towards you the public but towards the professionals.

The GMC, HCPC, GMC and NMC all protect the professionals.

Then there is the Professional Standards Agency who apparently have no powers to intervene. The Professionals Standards Agency are supposed to be responsible for overseeing all these agencies but I have just contacted them to hear they have no power under legislation to act. No wonder there is such unaccountability.

If there is no accountability what is the point of any codes of conduct or any of these agencies which cost the public a great deal of money yet fail to protect them/the vulnerable people. Iif nothing can be enforced to protect thousands of vulnerable people trapped in dreadful institutions and being abused all over this dreadful country then the Government surely needs to act. All the MP locally is contact the Trust. You will then get a standard letter and everything continues to go on and nothing is ever resolved so it is a waste of time. However our MP happens to be Health Secretary which is why I am turning to her not only for the sake of my daughter but so many others nationwide.

The most prominent people standing in the way of visits and contact appear to be DR WAQQAS KHOKHAR, the Responsible Clinician for Castle Ward and Emily Scott, Clinical Lead but then there are those at the very top namely Sarah Connery CEO, there is also the Management of the ward. Noone is taking the law into account and all hiding behind the MDT instead of being accountable individual or being made to review their actions according to their own code of conducts of which they are in breach. I am told not to contact the Carers Champion any more, all correspondence to be sent via the Care Concerns email address for which you do not get response when it comes to your questions as a whole.

From: Christopher Reid <Chris.Reid@parliament.uk>
Sent: 22 January 2024 14:55
To: susanb255
Subject: Re: Letter from Sarah Connery via Victoria Atkins MP (Case Ref: VA18567)

Dear Ms Bevis, 

Thank you for your response. 

As you are aware, we have previously raised your concerns about the wider issues with mental health and families with Victoria’s ministerial team, We are still waiting to hear back from them about this, however will of course let you know as soon as we do.

of course if you change your mind and want us to go back to the Trust on your daughter’s specific case them please do let us know.

Yours Sincerely,

Christopher Reid
Senior Caseworker
Office of the Rt Hon Victoria Atkins MP
Member of Parliament for Louth & Horncastle
Secretary of State for Health and Social Care

House of Commons                                       London SW1A 0AA   01507 527017

In line with data protection regulations, the Office of Victoria Atkins MP processes your personal data for casework and policy enquiry purposes. Please see our privacy notice at www.victoriaatkins.org.uk/privacy-notice.

________________________________________
From: susan bevis
Sent: 22 January 2024 12:38
To: REID, Chris <chris.reid@parliament.uk>
Subject: Re: Letter from Sarah Connery via Victoria Atkins MP (Case Ref: VA18567)

Dear Mr Reid

It is a waste of time going back to Trust Offices. I would like this whole issue of vulnerable people being sent far away from families out of area and kept a prisoner on MH wards for years and years dealt with in Parliament.  This is Victoria’s area and I know other cases and there needs to be more options.  Instead of bullying families and carers why not involve them in projects and set up something like Simon Trust.  There needs to be something done about the MHA and MCA as this is being abused.  There needs to be facility provision close to families and laws on accountability especially to Responsible clinicians who can lie as I can well and truly prove.  There needs to be restriction on length of time spent on acute wards.   When ms Connery speaks of 70 emails that is ridiculous.  In East Lindsay there is hardly anything in terms of facilities.  

I have not had anything in terms of satisfactory response.  The court system too is a disgrace.  Courts should be open and transparent.

I do not like to see human rights and other law being abused.

I would like to see more protection towards vulnerable people and their rights in hospitals and care homes and have been reading the paper just out on visiting rights etc.

All of this I would like to be addressed nationwide.

There needs to be accountability especial towards those at the top of Trusts and the Responsible Clinicians employed by a Trust.  For instance it is wrong for staff by way of instructions to act ultra vires, to use severance of the tiniest bit of leave to hospital shop, to take phone away, to use police to threaten to discourage family contact and worst of all day things like “I am having to ban you indefinitely ms bevis on the grounds *************************  stated dr Waqqas Khokhar on 28 December 2023.

Regards

Susan Bevis 

In all this time no Impact Assessment has been carried out. This is NHS Guidelines. Secondly the Government paper on visiting wards and care homes is completely forgotten by LPFT. They are rated good by the CQC and in all this time the CQC who describe themselves as a “business” have done nothing. The matter has also been referred to other agencies too responsibility for those employed by this Trust who say constantly “IT IS AN MDT DECISION” - No! it is not an MDT Decision if you read the details of their Code of Conduct. When I mention this they have no comment to say whatsoever and I am sure that many are just going along with instructions for the sake of their jobs.

I have nothing to hide which is why I am writing openly and honestly on here about the dreadful cruel and abusive NHS and how they treat the most vulnerable people in this country with no accountability whatsoever.   When I say “how would you feel if you were treated this way and had every phone call listened to and people dutifully writing notes that are not nice no doubt behind your back.” It is both undignified and degrading. Also this punishment is affecting others in the family too.

Eizabeth has spent years held like a prisoner on acute wards by LINCOLNSHIRE PARTNERSHIP TRUST who launched a campaign of bullying. When you phone it takes ages to get through on the phone sometimes. You then speak to a nurse or HCA and they cannot put you through to the phone that we as a family pay for. This has been going on for a very long time now. I think the contact through Vodafone is something like £13 a month but there is no usage because Elizabeth’s phone is locked away and they try to make out that there is a policy in place that is the same for other people but that is not true. I know this because friends on the ward were helping Elizabeth to contact me.

Last night I phoned the ward. After three attempts of not even being able to hear Elizabeth finally I got to speak to her on the ward phone. Her phone is left uncharged in the locker and they try to make out that she has access to it. All the time LINCOLNSHIRE PARTNERSHIP TRUST is discouraging and blocking calls to her mobile in the most disgusting manner. All the time they get away with it because the CQC and other agencies involved who I will feature later on do absolutely nothing. In an area where we have encountered nothing but bullying it is easy to see why staff are afraid to speak up.

Subject: Epilepsy & Psychosis

If Elizabeth has epilepsy she should not be treated with prn benzos for rapid tranquilisation. Prolonged and repeated use of benzodiaepines can increase the risk of rebound seizures or interictal epileptiform discharges (IEDs) in some individuals.

Schizophrenia-like symptoms are observed in some patients and are associated with epileptiform discharges but not overt seizures. The good response to antiepileptic treatment could be interpreted in the context of a (para)epileptic pathomechanism. 

“The EEG alterations might be due to a polygenetic effect due to different genes”.

This is why accurate diagnosis is so important.  You will see in the case below that a patient with schizophrenia like symptoms had epilepsy and recovered when taken off antipsychotics and treated with anti-convulsants. 

The idea that schizophrenia is ‘confirmed’ by daily observations conducted by unqualified staff is absurd.  Care assistants cannot possibly know how to differentiate between IEDs and psychosis induced by other causes.    This is why PANSS and associated physiological testing is crucial.  LPFT are in the dark ages when it comes to diagnosing and treating psychiatric patients. They neglect proper investigation of genetic markers in psychosis, they neglect EEG examination, they neglect genetic testing for treatment refractivity, they neglect investigation the potential inflammatory causes of brain disturbances and the ignore ADRs.

This indicates an ideological approach to diagnosing and treating psychosis rather than a medical one.  Belief based medicine, not evidence based medicine.     

See paper below.  It has some interesting comment on Clozapine you may like.  Reference 16 in the bibliography is to a paper that indicates that Clozapine can actually induce epilepsy in some patients due to a genetic polymorphism.  LPFT do not test for that either. 

Schizophrenia Associated with Epileptiform Discharges without Seizures Successfully Treated with Levetiracetam

Dominique Endres¹ Evgeniy Perlov¹ Bernd Feige¹ Dirk-Matthias Altenmüller² Nils Venhoff³ Ludger Tebartz van Elst¹*

• ¹Section for Experimental Neuropsychiatry, Department of Psychiatry, Faculty of Medicine, University of Freiburg, Freiburg, Germany
• ²Freiburg Epilepsy Center, Department of Neurosurgery, Faculty of Medicine, University of Freiburg, Freiburg, Germany
• ³Department of Rheumatology and Clinical Immunology, Faculty of Medicine, University of Freiburg, Freiburg, Germany

Background: Schizophrenia-like disorders can be divided into endogenic or primary, idiopathic, polygenetic forms, and different secondary, organic subgroups [e.g., (para)epileptic, immunological, degenerative]. Epileptic and paraepileptic explanatory approaches have a long tradition due to the high rate of electroencephalography (EEG) alterations in patients with schizophrenia.

Case presentation: We present the case of a 23-year-old female patient suffering, since the age of 14 years, from a fluctuating paranoid-hallucinatory syndrome with formal thought disorder, fear, delusions of persecution, auditory, visual, and tactile hallucinations, as well as negative and cognitive symptoms. Laboratory measurements showed increased titers of antinuclear antibodies (ANAs) in the context of ulcerative colitis. While there was no clear history or evidence of epileptic seizures, the EEG showed generalized 3 Hz polyspike wave complexes. Under treatment with levetiracetam, the symptoms disappeared and the patient was able to complete vocational training.

Conclusion: The schizophrenia-like symptoms associated with epileptiform discharges but not overt seizures and the good response to antiepileptic treatment could be interpreted in the context of a (para)epileptic pathomechanism. The EEG alterations might be due to a polygenetic effect due to different genes. Mild immunological mechanisms in the framework of ulcerative colitis and increased ANA titers might have supported the network instability. This case report illustrates (1) the importance of EEG screenings in schizophrenia, (2) a potential pathogenetic role of epileptiform discharges in a subgroup of patients with schizophrenia-like symptoms, and (3) that antiepileptic medication with levetiracetam could be a successful treatment alternative in schizophrenia-like disorders with EEG alterations.

Background

Schizophrenia-like disorders are characterized by delusional perception and delusions of control, hallucinations (e.g., commenting or discussing voices), thought insertion or withdrawal, cognitive impairment, thought disorders, or social withdrawal.¹ In addition to primary, endogenic or idiopathic, polygenetic forms, different secondary pathophysiological mechanisms [e.g., (para)epileptic, immunological, degenerative] can be assumed. Because of the high rates of electroencephalography (EEG) alterations, ranging from 7 to 60% in patients with schizophreniform syndromes, epileptic and paraepileptic explanatory approaches have a long tradition (1–3). In line with this assumption, we reported the first case of a young patient with a schizophrenia-like disorder, generalized spike-and-slow-wave complexes without epileptic seizures but with remission under treatment with valproate (4, 5). Immunological reasons might be due to autoantibody-associated autoimmune encephalitis, cerebral vasculitis, or collagenosis [e.g., systemic lupus erythematosus (SLE)] (6). Immunological effects might lead to network instability and therefore cause (para)epileptic phenomena (7). The detection of a (para)epileptic or immunological mechanism opens new treatment perspectives, in that antiepileptics or immunomodulators may be helpful (4, 5, 7–10).

Case Presentation

Clinical Presentation

We present the case of a 23-year-old female office clerk suffering from fluctuating paranoid-hallucinatory symptoms since the age of 14 years (2007). Therefore, the diagnosis of paranoid schizophrenia was made by different psychiatrists. Although taking neuroleptics, in the course of the disease, the patient developed five episodes (for several weeks) with paranoid-hallucinatory exacerbation. In these episodes, the patient suffered from formal thought disorder, fear, delusions of persecution, auditory hallucinations with commenting, discussing, and commanding voices, visual hallucinations with seeing maggots in her room, and tactile hallucinations with the feeling of being touched from behind. In parallel to these exacerbations, the patient developed severe negative and cognitive symptoms including attention and memory deficits, fatigue, depressive mood, and sleep disturbances thus completing the psychopathological features of comprehensive schizophrenia. Neurological and medical examinations were normal.

Family History

There was a positive family history for unipolar depression, which was diagnosed earlier in two sisters, both parents, and both grandmothers. There was no history for schizophrenia-like psychopathology, bipolar disorder, or epilepsy.

Somatic and Developmental History

Symptoms started 6 weeks after pain of the large joints. Therefore, a rheumatological disease was discussed. During an external work-up of repeated diarrhea, a chronic inflammation gut disease (ulcerative colitis) was diagnosed in 2014 and treated with mesalazine. No birth complications or in utero abnormalities were remembered; the birth was performed by cesarean section. The early childhood development was normal. No febrile convulsions or inflammatory brain diseases were remembered. The patient suffered mild cerebral contusions at the age of 4 and 12 years.

Diagnostic Findings

The diagnostic findings are summarized in Table 1. Taken together, the immunological alterations were compatible with the previously known ulcerative colitis (11). The electrophysiological findings (Figure 1) would be compatible with primary (idiopathic) generalized epilepsy; however, the history for epileptic seizures including absences and myoclonic jerks was negative.

Table 1

Figure 1. Frontal accentuated intermittent rhythmic delta activity (FIRDA, left) and generalized 3 Hz polyspike wave complexes (middle) in the bipolar longitudinal rows (7 µV/mm, 0.3 s, 70 Hz). The findings of the independent component analysis are presented in the right picture [the following four relevant components were found, left: activity traces, with examples of atypical activity cut from the clinical electroencephalography and appended at the dotted lines. Right: topographies, nose upward, negative (direction opposite of activity trace) blue, positive (direction same as activity trace) red. Right (component 3) and left (component 5) frontal activity show most prominent ~2.6 Hz bursts. Higher frequency activity frontocentral (component 2) and occipital (alpha component 7) are partially related].

Differential Diagnosis

The schizophreniform symptoms fulfilled the criteria of paranoid-hallucinatory schizophrenia (see footnote 1). Therefore, the most important differential diagnoses would be schizophrenia plus coincidental epileptiform discharges. Although the findings of the investigation led us to our consideration of neuropsychiatric SLE, the American College of Rheumatology classification criteria for SLE were not fulfilled.²

Therapy and Outcome

External neuroleptic treatment with risperidone (4 mg), amisulpride (600 mg), perazine (100 mg), aripiprazole (15 mg), and clozapine (275 mg) did not lead to long-term stabilization. Additional treatment with fluoxetine (20 mg) and citalopram (20 mg) for affective, negative, and cognitive symptoms did not successfully improve these symptoms. During the first visit in our clinic, in 2013, we detected the abovementioned epileptiform discharges. Assuming a (para)epileptic pathomechanism, we added antiepileptic treatment with valproate (1,500 mg) to the neuroleptic medication with clozapine and aripiprazole. At this point, the cognitive deficits improved significantly. Also, the EEG improved except for the (F)IRDAs. Another paranoid-hallucinatory episode in 2014 was treated successfully with a dose increase of clozapine and valproate. Because of a strong weight gain, the therapy with valproate was changed to topiramate (200 mg) in 2014. Assuming a (para)epileptic pathomechanism, clozapine was reduced and stopped in 2014. Aripiprazole was reduced in January 2014 and stopped in 2015. Normal results were found in both the routine EEG and in the EEG after sleep deprivation (2014). In the further course, topiramate led to a severe loss of appetite and was therefore changed to levetiracetam (1,500 mg) in 2014. The mental condition stabilized with the short-term antiepileptic treatment with topiramate and the subsequent antiepileptic treatment with levetiracetam (since 2014, and since 2015 as monotherapy). There were no more paranoid-hallucinatory episodes, the negative symptoms declined, the patient became a mother (in the spring of 2016); she lived alone, took care of her daughter, and simultaneously finished her vocational training (in the summer of 2016). She was able to suspend the mesalazine therapy and therefore only took levetiracetam (1,500 mg) at the time of stabilization.

Discussion

We present the case of a patient with a schizophrenia-like disorder and, following our judgment, a (para)epileptic pathomechanism, because of the distinct epileptiform discharges without seizures and remission under the anticonvulsive treatment with topiramate and subsequently levetiracetam monotherapy.

Reason and Potential Pathophysiology of Network Instability

The EEG alterations might be due to a polygenetic effect caused by different genes (12). The immunological mechanisms in the framework of ulcerative colitis and increased antinuclear antibody titers might have supported the network instability by mild inflammatory processes (7, 13–15). Medication might also disclose underlying polygenetic or immunological network instability (16). The local area network inhibition (LANI) hypothesis might explain the causal relationship between epileptiform EEG discharges and schizophrenia-like symptoms. Excitatory network activity, as represented by the 3 Hz polyspike wave complexes, might lead to consecutive inhibitory processes in a physiological attempt of the central nervous system to stabilize the excitatory–inhibitory equilibrium of local cerebral networks. The repetitive excitatory activity, as documented by consecutive EEGs in our patient, could have exceeded a critical threshold, leading to the successive hyperinhibition of cerebral networks. Following the LANI hypothesis, the symptoms are due to the secondary induced processes of hyperinhibition (e.g., temporal hyperinhibition might have led to auditory hallucinations or memory deficits) (2–5, 17).

Treatment Considerations

Following the LANI hypothesis, the cognitive improvement after the addition of valproate to the neuroleptic treatment would be explained by the reduced epileptic activity and therefore the subsequent amelioration of inhibitory processes. In line with this assumption, comprehensive long-term stabilization was not achieved by several attempts of neuroleptic medication alone in spite of clear and very convincing effects of the treatment with clozapine in particular on positive symptoms. However, such a comprehensive improvement and even full remission was achieved with topiramate and later levetiracetam monotherapy. Thus, clozapine with its well-known proconvulsive properties might well have counteracted inhibitory processes, while it is at the same time most likely unable to improve causative excitatory neuronal activity. By contrast, by reducing the epileptiform activity, topiramate and levitiracetam monotherapy might have resulted in a more causal and therefore more comprehensive improvement of relevant pathophysiology. Earlier, we published a case of a (para)epileptic schizophrenia-like disorder successfully treated with valproate (4). Valproate, and likewise lamotrigine, is already established as an augmentative treatment strategy in schizophrenia (18). One might hypothesize that patients with (para)epileptic pathomechanisms will benefit significantly more from antiepileptic treatment than other subgroups. To our knowledge, this is the first published case study that describes a patient with a schizophrenia-like disorder who was successfully treated with levetiracetam. Levetiracetam is rarely used off-label in psychiatry probably because of its potential side effects, such as agitation, aggression, fear, and psychosis (2). The advantage of levetiracetam is that it can be rapidly dosed up to effective concentrations. Therefore, on a single case basis, the working hypothesis of a (para)epileptic pathomechanism could be tested quickly. In comparison, valproate effects could be due to combined γ-aminobutyric acid (GABAergic) and antiglutamatergic effects, and lamotrigine effects might be due to potential antiglutamatergic effects. However, the mechanism of levetiracetam cannot be explained by such direct transmitter effects. The effects of levetiracetam seem to be associated with the binding of the synaptic vesicle glycoprotein 2A (SV2A) (2). SV2A can be found in presynaptic membranes; it controls the calcium-dependent exocytosis of different neurotransmitters into the synaptic gap (19, 20). Therefore, it might also influence GABAergic and glutamatergic transmission (21).

Limitations

Epileptiform discharges are found in less than 1% of healthy adults (1, 22–24) and as a rare consequence of clozapine treatment (16). Therefore, the EEG alterations could be interpreted either as an incidental finding in a patient with schizophrenia or as a clozapine side effect. However, the clinical course—with improvement under antiepileptic treatment in parallel with EEG normalization—speaks against the assumption. The pathophysiological processes might be explained by the LANI hypothesis; however, this is only an unproven, theoretical framework that needs further investigation.

Conclusion

This case report illustrates the idea of a possible (para)epileptic pathomechanism in a patient with a schizophrenia-like disorder. Regarding diagnostic procedure, our case shows the importance of EEG examinations in typical schizophrenia-like disorders. Regarding pathophysiology, the case illustrates a potential pathogenetic role of epileptiform discharges in a subgroup of patients with schizophrenia-like symptoms. Regarding treatment, the case demonstrates that anticonvulsive medication with levetiracetam and also topiramate or valproate could be a successful treatment alternative in schizophrenia with EEG alterations.

Ethics Statement

The patient has given her informed and written consent for this case report, including the presented images, to be published.

Author Contributions

LTvE treated the patient. DE wrote the paper and performed the data collection. DE and LTvE performed the interpretation of the diagnostic findings and therapy effects. BF performed and interpreted the EEG analysis. NV performed and interpreted the immunological analyses. EP and D-MA reviewed the diagnostic results and contributed to the manuscript preparation. All the authors were significantly involved in the theoretical discussion and the preparation of the manuscript, and they read and approved the final version of the manuscript.

Conflict of Interest Statement

DE, EP, and BF: none; D-MA: lecture fees from UCB Pharma; NV: advisory boards, lectures, research, or travel grants within the last 3 years: Janssen-Cilag, Roche, Novartis, AbbVie, GSK, and Medac. LTvE: lectures, work shops, or travel grants within the last 3 years: Eli Lilly, Medice, Shire, UCB, Servier, and Cyberonics.

Abbreviations

ACR, American College of Rheumatology; ANA, antinuclear antibody; CSF, cerebrospinal fluid; EEG, electroencephalography; FIRDA, frontal intermittent rhythmic delta activity; GABA, γ-aminobutyric acid; HV, hyperventilation; ICA, independent component analyses; IRDA; intermittent rhythmic delta activity; LANI, local area network inhibition; SLE, systemic lupus erythematosus; SV2A, synaptic vesicle glycoprotein 2A.

Footnotes

1. ^http://apps.who.int/classifications/icd10/browse/2010/en#/F20-F29.
2. ^www.rheumatology.org/Portals/0/Files/1997%20Update%20of%201982%20Revised.pdf.

References

1. Shelley BP, Trimble MR, Boutros NN. Electroencephalographic cerebral dysrhythmic abnormalities in the trinity of nonepileptic general population, neuropsychiatric, and neurobehavioral disorders. J Neuropsychiatry Clin Neurosci(2008) 20:7–22. doi: 10.1176/appi.neuropsych.20.1.7

PubMed Abstract | CrossRef Full Text | Google Scholar

2. Tebartz van Elst L, Perlov E. Epilepsie und Psyche: Psychische Störungen bei Epilepsie – epileptische Phänomene in der Psychiatrie. 1st ed. Stuttgart: Kohlhammer (2013).

Google Scholar

3. Endres D, Perlov E, Feige B, Fleck M, Bartels S, Altenmüller D, et al. Electroencephalographic findings in schizophreniform and affective disorders. Int J Psychiatry Clin Pract (2016) 16:1–8. doi:10.1080/13651501.2016.1181184

PubMed Abstract | CrossRef Full Text | Google Scholar

4. van Elst LT, Schulze-Bonhage A, Altenmüller D, Ebert D. Generalised spike-and-slow-wave complexes without seizures in schizophrenia. Br J Psychiatry (2011) 199:253–4. doi:10.1192/bjp.199.3.253a

CrossRef Full Text | Google Scholar

5. Tebartz van Elst L, Krishnamoorthy ES, Schulze-Bonhage A, Altenmüller D, Richter H, Ebert D, et al. Local area network inhibition: a model of a potentially important paraepileptic pathomechanism in neuropsychiatric disorders. Epilepsy Behav (2011) 22:231–9. doi:10.1016/j.yebeh.2011.06.016

PubMed Abstract | CrossRef Full Text | Google Scholar

6. Endres D, Perlov E, Dersch R, Baumgartner A, Hottenrott T, Berger B, et al. Evidence of cerebrospinal fluid abnormalities in patients with depressive syndromes. J Affect Disord (2016) 198:178–84. doi:10.1016/j.jad.2016.03.030

PubMed Abstract | CrossRef Full Text | Google Scholar

7. Tebartz van Elst L, Stich O, Endres D. Depressionen und Psychosen bei immunologischen Enzephalopathien. PSYCH up2date (2015) 9(05):265–80. doi:10.1055/s-0041-102941

CrossRef Full Text | Google Scholar

8. van Elst LT, Klöppel S, Rauer S. Voltage-gated potassium channel/LGI1 antibody-associated encephalopathy may cause brief psychotic disorder. J Clin Psychiatry (2011) 72:722–3. doi:10.4088/JCP.10l06510

CrossRef Full Text | Google Scholar

9. Endres D, Perlov E, Stich O, Rauer S, Waldkircher Z, Lange T, et al. In vivo hypoglutamatergic state is associated with reduced cerebral glucose metabolism in anti-NMDA receptor encephalitis. BMC Psychiatry (2015) 15:186. doi:10.1186/s12888-015-0552-4

CrossRef Full Text | Google Scholar

10. Endres D, Perlov E, Stich O, Tebartz van Elst L. Steroid responsive encephalopathy associated with autoimmune thyroiditis (SREAT) presenting as major depression. BMC Psychiatry (2016) 6:184. doi:10.1186/s12888-016-0897-3

PubMed Abstract | CrossRef Full Text | Google Scholar

11. Barahona-Garrido J, Camacho-Escobedo J, García-Martínez C, Tocay H, Cabiedes J, Yamamoto-Furusho J. Antinuclear antibodies: a marker associated with steroid dependence in patients with ulcerative colitis. Inflamm Bowel Dis (2009) 15:1039–43. doi:10.1002/ibd.20852

PubMed Abstract | CrossRef Full Text | Google Scholar

12. Spillane J, Kullmann D, Hanna M. Genetic neurological channelopathies: molecular genetics and clinical phenotypes. J Neurol Neurosurg Psychiatry (2016) 87:37–48. doi:10.1136/jnnp-2015-311233

PubMed Abstract | CrossRef Full Text | Google Scholar

13. Hazouard E, Legras A, Diot E, Ferrandière M, Corcia P, Giniès G. [Cerebrospinal fluid complement and antinuclear antibodies in lupus meningoencephalitis]. Rev Neurol (Paris) (1998) 154:549–50.

PubMed Abstract | Google Scholar

14. Bonrath E, Rijcken E, Dziewas R, Vieth V, Bettenworth D, Senninger N, et al. [Cerebral vasculitis as rare extraintestinal manifestation in ulcerative colitis: review of the literature and case report]. Zentralbl Chir (2010) 135:350–3. doi:10.1055/s-0030-1247464

CrossRef Full Text | Google Scholar

15. Bechter K. Updating the mild encephalitis hypothesis of schizophrenia. Prog Neuropsychopharmacol Biol Psychiatry(2013) 42:71–91. doi:10.1016/j.pnpbp.2012.06.019

PubMed Abstract | CrossRef Full Text | Google Scholar

16. Treves I, Neufeld M. EEG abnormalities in clozapine-treated schizophrenic patients. Eur Neuropsychopharmacol (1996) 6:93–4. doi:10.1016/0924-977X(95)00057-V

PubMed Abstract | CrossRef Full Text | Google Scholar

17. Tebartz van Elst L, Fleck M, Bartels S, Altenmüller D, Riedel A, Bubl E, et al. Increased prevalence of intermittent rhythmic delta or theta activity (IRDA/IRTA) in the electroencephalogram (EEG) of patients with borderline personality disorder. Front Behav Neurosci (2016) 10:12. doi:10.3389/fnbeh.2016.00012

CrossRef Full Text | Google Scholar

18. Dold M, Leucht S. Pharmacotherapy of treatment-resistant schizophrenia: a clinical perspective. Evid Based Ment Health (2014) 17:33–7. doi:10.1136/eb-2014-101813

PubMed Abstract | CrossRef Full Text | Google Scholar

19. Lynch B, Lambeng N, Nocka K, Kensel-Hammes P, Bajjalieh S, Matagne A, et al. The synaptic vesicle protein SV2A is the binding site for the antiepileptic drug levetiracetam. Proc Natl Acad Sci U S A (2004) 101:9861–6. doi:10.1073/pnas.0308208101

CrossRef Full Text | Google Scholar

20. Zhang L, Li S, Li H, Zou X. Levetiracetam vs. brivaracetam for adults with refractory focal seizures: a meta-analysis and indirect comparison. Seizure (2016) 39:28–33. doi:10.1016/j.seizure.2016.05.004

PubMed Abstract | CrossRef Full Text | Google Scholar

21. Wood MD, Gillard M. Evidence for a differential interaction of brivaracetam and levetiracetam with the synaptic vesicle 2A protein. Epilepsia (2016). doi:10.1111/epi.13638 [Epub ahead of print].

PubMed Abstract | CrossRef Full Text | Google Scholar

22. Gregory RP, Oates T, Merry RT. Electroencephalogram epileptiform abnormalities in candidates for aircrew training. Electroencephalogr Clin Neurophysiol (1993) 86:75–7. doi:10.1016/0013-4694(93)90069-8

PubMed Abstract | CrossRef Full Text | Google Scholar

23. Bennett DR. Spike-wave complexes in “normal” flying personnel. Aerosp Med (1967) 38:1276–82.

Google Scholar

24. Thorner MW. Procurement of electroencephalograph tracings in 1000 flying cadets for evaluating the Gibbs technique in relation to flying ability. USAD School of Aviation Medical Research Report No. 7–1. (1942).

Google Scholar

Keywords: epilepsy, schizophrenia, epileptiform discharges, levetiracetam, paraepileptic, LANI hypothesis

Citation: Endres D, Perlov E, Feige B, Altenmüller D-M, Venhoff N and Tebartz van Elst L (2017) Schizophrenia Associated with Epileptiform Discharges without Seizures Successfully Treated with Levetiracetam. Front. Psychiatry 8:12. doi: 10.3389/fpsyt.2017.00012

Received: 27 October 2016; Accepted: 17 January 2017;
Published: 08 February 2017

Edited by:

Karl Bechter, University of Ulm, Germany

Reviewed by:

Sabina Berretta, Harvard Medical School, USA
Mark Cunningham, Newcastle University, UK

PANSS

The PANSS has been studied for its psychometric properties, and the data shows adequate Internal consistency, good test-retest reliability, and inter-rater reliability. In addition the PANSS has been researched in quality of life studies, functional status, natural history of schizophrenia and treatment outcomes. It has most of its evidence base to support its use for grading the severity of schizophrenia symptoms, staging of schizophrenia and treatment progress with medications.

The scale has mostly been used to inventory, grade and follow the symptoms in schizophrenia. It quantifies positive symptoms, which refer to an excess or distortion of normal functions (e.g., hallucinations and delusions), and negative symptoms, which represent a diminution or loss of normal functions. The PANSS is composed of 3 subscales: Positive Scale, Negative Scale, and General Psychopathology Scale. Each subscale is rated with 1 to 7 points ranging from absent to extreme. The range for the Positive and Negative Scales is 7-49, and the range for the General Psychopathology Scale is 16-112. The total PANSS score is simply the sum of the sub scales. In addition to these measures, a Composite Scale is scored by subtracting the negative score from the positive score. This yields a bipolar index that ranges from –42 to +42, which is essentially a difference score reflecting the degree of predominance of one syndrome in relation to the other.

The Positive and Negative Syndrome Scale (PANSS) was published in 1987 by Stanley Kay, Lewis Opler, and Abraham Fiszbein. It’s a scale used for measuring symptom severity of schizophrenia, and widely used in the study of psychopharmacologic therapy. The scale was based off the Psychopathology Rating Schedule (PRS) and the Brief Psychiatric Rating Scale (BPRS). The PANSS is a 30-item clinician-administered rating scale, but requires 45 to 50 minutes to be administered by a subject matter expert. The interviewer must be trained to a standardized level of reliability. The PANSS has been published officially across 40 languages and is used internationally in mostly clinical research.

PANNS is also used to deny patients autonomy (capacity) It is used to judge the diminution of loss of function by rating it on a scale. If LPFT do not use this scale how have they determined that ****** lacks capacity? LPFT state she has severe symptoms but have not measured them. The severity or otherwise seems to be based on the opinions of staff, some of whom are not medically qualified, never mind ‘subject matter experts’.

This is why the PANSS score is important. I do not need to agree with the diagnostics of schizophrenia to see the importance. The fact is that ****** been diagnosed with paranoid schizophrenia but LPFT have not used this metric in the diagnosis or the treatment they give her. LPFT prefer and have stayed reliant on subjective observations by multiple staff on a daily basis which is hardly a scientific method and effectively is a trial and error, hit and miss approach. PANSS is a doctors responsibility, not a ward care assistant’s.

Note that medication decisions are based on PANSS and so I am curious to know what are LPFT using in that case?

This is very similar to the ignoring of the metabolism issues. Whilst known that she is a poor metaboliser, :LPFT make no provision for it. So, they take no notice of the diagnostic criteria or notice of metabolism problems yet still label ****** with this ‘diagnosis’ and medicate her according to it being correct?

It has come to my attention the following:

“****** regular mental health medication is a Clopixol (Zuclopenthixol Decanoate) 400mg depot. This is administered once every two weeks and has been authorised by a Second Opinion Appointed Doctor on 29th December 2023 as well as being supported by ******** Responsible Clinician.

-LPFT does not routinely use the Positive and Negative Syndrome Scale for Schizophrenia (PANSS). This was confirmed by the Responsible Clinician who has stated that ******** progress is currently being judged based on engagement with staff and activities.”

Finally I do not appear to have response to my previous email about visiting the ward on the 12 February and ****** phoned me today. Please explain about Sheffield. I was not clear whether this is another placement or what? ****** has shared with me she is thought to have epilepsy and that Dr S came to see her. Can you please advise how things went and the outcome? ****** said that it was needed a recording of the episode which she had another one the other day. It is not good that my daughter is injected after every episode. This is affecting her sleep pattern and it is affecting her blood oxygen levels. Rapid tranquilisations on a frequent basis are not good for my daughter’s physical health and may even be causing the problem of episodes rather than suggestions that I am contributory. I have not been allowed to see ****** for months so how can this be any way contributory to me? On the Advanced Declaration it clearly says that ****** does not wish to be subject to unnecessary treatments and rapid tranquilisations fit into that description. Please note that the rapid tranquilisations are not part of my daughter’s “treatment” and should therefore cease. I do not want to hear that everything has been agreed by the SOAD. In fact the SOAD needs to be aware of the above and so do the CQC.

I would suggest that LPFT contact Cygnet Durham where Dr M was witness to such episode as there may be a recording of that under Cygnet.

As someone who has attained qualifications re Best Interest I can now judge that nothing has been done correctly under LPFT, especially the capacity assessments along with the PANSS score.

From: susan bevis Sent: 07 February 2024 22:45

To: CARECONCERNS (LINCOLNSHIRE PARTNERSHIP NHS FOUNDATION TRUST) <lpft.careconcerns@nhs.net>

Cc: Enquiries <Enquiries@cqc.org.uk>

Subject: PANSS SCORE – *********** – For the Attention of Sarah Connery, Kevin Lockyer and Emily Scott (Clinical Lead)