Innov Clin Neurosci. 2024;21(10–12):8.
Dear Editor:
The interesting article by Zuckerberg et al1 on a 29-year-old male patient with schizophrenia, catatonia, and stupor associated with an enlarged cavum septum pellucidum (CSP), which only responded to electroconvulsive therapy (ECT), raises concerns that should be discussed.
The first point is that a single case does not allow general conclusions to be drawn. To assess whether enlarged CSP is indeed related to psychiatric disorders, prospective, controlled multicenter studies are needed. However, enlarged CSP has been repeatedly reported in association with organic catatonia and secondary causes of schizophrenia (pseudo-schizophrenia).2,3
The second point relates to the delay in the administration of ECT.1 The delay was explained by the lengthy process of obtaining permanent guardianship in the absence of available family members. However, two sentences later it is stated that the patient did not respond to the staff but to his family.1 This discrepancy should be clarified. Since catatonia and stupor, regardless of cause, constitute an emergency requiring urgent, comprehensive neurologic, internal medicine, and psychiatric evaluation and treatment, permission for ECT could have been granted more quickly by the patient’s legal representative.
The third point is that only a scant explanation was given for the severe episode of agitation or delirium at the second hospital, where the patient required four-point restraints. Was this due to the underlying psychiatric syndrome, side effects of the current medication, or seizures? We should also be informed about the patient’s cognitive status (e.g., orientation, memory attention) when not catatonic.
The fourth point is that causes of catatonia other than schizophrenia have not been sufficiently ruled out. In addition to schizophrenia, catatonia can be due neurological disease, psychiatric syndromes, or an internal disease. Neurological diseases associated with catatonia include neuroleptic malignant syndrome, autoimmune encephalitis, neuroborreliosis, cerebral vasculitis, multiple sclerosis, ischemic stroke, progressive multifocal leukoencephalopathy (PML), infectious encephalitis or meningitis, traumatic brain injury, etc.4 Psychiatric causes of catatonia other than schizophrenia include major depression, bipolar disorder, post-traumatic stress disorder (PTSD), or anxiety disorders.4 Internal causes of catatonia can include kidney failure, lupus erythematosus, thyroid hormonal dysfunction, substance withdrawal, electrolyte disorders, or hormonal disturbances.4 All these differential causes of catatonia must be thoroughly clarified before attributing them to schizophrenia.
The fifth point is that the cerebrospinal fluid (CSF) tests were inadequate. There is no mention of the results of the virus panel, particularly whether severe acquired respiratory syndrome coronavirus-2 (SARS-CoV-2) was positive or negative, and lactate, interleukins, chemokines, glial factors, tau, 14-3-3 protein, proteins of serpin pathways, complement factors, glycoprotein-alpha-2, glycoprotein-alpha-1, linear and circular ribonucleic acids, or light chains are also not mentioned. Although the initial CSF examination showed no evidence of CSF inflammation, subsequent examinations might have revealed autoimmune encephalitis or infectious encephalitis. The study also lacks the antibodies associated with immune encephalitis, which are positive in about half of cases.
The sixth point is that the patient did not undergo brain magnetic resonance imaging (MRI) with contrast medium to rule out infections or immune encephalitis, brain magnetic resonance angiography (MRA), brain computed tomography angiography (CTA), brain magnetic resonance venography (MRV), or brain magnetic resonance spectroscopy (MRS) to determine whether there was a vascular problem, such as reversible cerebral vasoconstriction syndrome (RCVS), dissection of cerebral arteries, occlusion of cerebral arteries, aneurysm formation, or venous sinus thrombosis.1 It would also have been desirable to know whether there was a lactate peak, a reduced N-acetyl aspartate peak, or an increased glutamate peak.
The seventh point is that no family history was provided.1 Since schizophrenia, stupor, and catatonia can have a genetic background,5 it would have been mandatory to report whether any of the first-degree relatives suffered from a psychiatric or neurologic disorder.
A last point is that there was no exclusion of a SARS-CoV-2 infection or complications of a SARS-CoV-2 vaccination.6 No blood gas analysis results were provided.
It should also be noted that a physician who does not have resources to adequately investigate psychosis or catatonia should diagnose psychosis not otherwise specified or catatonia not otherwise specified, but should never label the patient with schizophrenic catatonia without a full diagnostic march.
In conclusion, patients with catatonia require immediate comprehensive neurologic and psychiatric examinations not to miss any of the many differential causes.
References
- Zuckerberg A, Pothen N, Fitzsimmons A. Genesis of mental disorders: could it be cavum septum pellucidum (CSP) et vergae? a case report of CSP in schizophrenia with catatonia. Innov Clin Neurosci. 2024;21(1–3):63–65.
- Marques JG. Temporal lobe epilepsy mimicking schizoaffective disorder in patients with cavum septi pellucidi. Prim Care Companion CNS Disord. 2020;22(6):20l02613.
- Gama Marques J. Schizophrenia misdiagnosis after capgras and cotard delusions in a patient with infantile cystinosis, cavum septi pellucidi, cavum vergae and cavum veli interpositi. Behav Sci (Basel). 2023;13(2):157.
- Heckers S, Walther S. Catatonia. N Engl J Med. 2023;389(19):1797–1802.
- Ishikawa M, Omachi Y, Sato N, Nakagawa E. Bipolar disorder in megalencephalic leukoencephalopathy with subcortical cysts: a case report. BMC Psychiatry. 2020;20(1):349.
- Florek S, Sołtys W, Bielówka M, Kołodziejska A. Catatonic syndrome during COVID-19 – a case study. Psychiatr Pol. 2023;57(5):1001–1010.
With regards,
Josef Finsterer, MD, PhD
Dr. Finsterer is with Neurology & Neurophysiology Center in Vienna, Austria.
Funding/financial disclosures. The author has no conflicts of interest relevant to the content of this letter. No funding was received for the preparation of this letter.
