Anti-NMDA-Receptor encephalitis is a severe form of encephalitis that was recently identified in the context of acute neuropsychiatric presentation. Here, we describe the case of a 17-year-old girl referred for an acute mania with psychotic features and a clinical picture deteriorated to a catatonic state. Positive diagnosis of anti-NMDA-receptor encephalitis suggested specific treatment. She improved after plasma exchange and immunosuppressive therapy. Post-cognitive sequelae (memory impairment) disappeared within 2-year follow-up and intensive cognitive rehabilitation.
NMDA receptors are ligand-gated cation channels that play an important role in synaptic plasticity [1] and seem to be implicated in the physiopathology of neuropsychiatric disorders [2]. NMDA receptors are heteromers of NR1 and NR2 subunits (A, B, C or D) that bind glycine and glutamate, respectively [3]. Both glycine and glutamate must bind for the NMDA receptor to be functional. Anti-NMDA-receptor encephalitis has been recently identified. The antibodies found in anti-NMDA-receptor encephalitis are directed against the NR1 subunit of the NMDA receptor [4].
The clinical syndrome of a paraneoplastic neuropsychiatric disorder associated with ovarian teratoma was first described in 2005 [5], and Dalmau and colleagues identified and described the specific antibody in 2007 [6]. Since then, several case reports of anti-NMDA-receptor encephalitis have been published, suggesting that this illness is not rare [4,7,8,9,10,11]. In 2008, Dalmau and al. published a series of 100 cases of anti-NMDA-Receptor encephalitis [12]. Recently, the same group reported on more than 400 patients with anti-NMDA-Receptor encephalitis over a 3-year period [4]. The exact incidence of anti-NMDAR encephalitis is unknown, but it seems to be more frequent than any other known paraneoplastic encephalitis [4]. It predominantly affects children and young adults and may occur with or without tumor association [4]. Eighty percent of the patients are women. The clinical syndrome is now clearly described. First, a brief viral-like episode (e.g., headache, hyperthermia) can occur. This is followed by an acute phase that includes neuropsychiatric symptoms such as agitation, psychotic symptoms (i.e., delusions or hallucinations), behavioral changes, generalized or partial seizures, progressive unresponsiveness, abnormal movements (e.g., dyskinesia), dysautonomy and hypoventilation that can require ventilation assistance and intensive care. The frequency of tumors varies according to age, sex and ethnicity [4]. Usually teratoma of the ovaries in women or testicular tumors in men that express NMDA-R which triggers antibody production, are found [13].
For patients with anti-NMDA-Receptor encephalitis, magnetic resonance imaging (MRI) scans are often normal or show only minor, non-specific signs. Patients' cerebrospinal fluid (CSF) may show pleocytosis and an elevated protein concentration. In addition, patients' electroencephalogram (EEG) results exhibit diffuse slow activity. Despite a severe initial presentation, complete or near complete recovery can be reached using immunosuppressive therapy and tumor resection; however, severe sequelae and even death occur in up to 25% of all cases [12].
In this paper, we present a case report of a 17-year-old girl referred for acute mania with psychotic features and malignant catatonia due to anti-NMDA-Receptor encephalitis. She was first treated empirically with immunosuppressive therapy and plasma exchange (PE) for presumed immune mediated encephalitis based on increased antinuclear antibodies. Treatment was then continued based on the diagnosis of anti-NMDA-R encephalitis.
Case Presentation
A 17-year-old girl with no medical, psychiatric or surgical history began exhibiting symptoms of hypochondriasis. Her parents reported that she had sudden changes of mood, becoming more irritable and sensitive. In a few days, she began to get worse. She presented manic symptoms with psychomotor excitement, logorrhea, tachypsychia, euphoric state and insomnia. She had delusions and hallucinations with dysmorphophobic and nosophobic thematics. She also presented with one generalized seizure, although she did not suffer from epilepsy.
The patient was transferred to the closest psychiatric department where she presented with catatonia syndrome without extrapyramidal signs. She was given olanzapine (40 mg/day), loxapine (50 mg/day) and clonazepam (3.5 mg/day). She soon showed malignant catatonia with autonomic instability, fever, arterial hypertension and CPK increase (4500 UI/L) and was transferred to the university department of adolescent psychiatry. Antipsychotic medications were stopped, and a high dosage of lorazepam (15 mg/day) was started. Because of her life-threatening condition, the patient was transferred to an intensive care unit. Dysautonomy and fever improved, but she remained catatonic, showing rigidity, mutism, staring, waxy flexibility and negativism. An exhaustive biological check-up was conducted to rule out possible organic causes (i.e., immunological, infectious, metabolic, iatrogenic and toxic) [14]. An examination of her cerebral spinal fluid revealed eight cells, and an electroencephalogram showed diffuse slow waves (0.5 to 1 wave per second); antinuclear factors were positive (1/320), but anti-DNA antibodies were not. A Magnetic Resonance Imaging (MRI) scan showed subtle, small and non-specific hyperintensities (Figure1). A cerebral positron emission tomography (18FDG-PET) revealed left frontal-temporal cortex hypometabolism and moderate bilateral hippocampic hypometabolism (Figure2). Electroconvulsive therapy (ECT) was postponed due to arguments supporting hypothesis of acute encephalitis (seizures, EEG signs and brain hypometabolism). Based on suspicion of neuropsychiatric systemic lupus erythematosus (SLE) (because of positive antinuclear factors and neurological symptoms), immuno-suppressive therapy was initiated. For 3 days, she received prednisone at a dose of 1 g IV. This was followed by a month of 1 mg/kg/day oral prednisone, which was progressively decreased. Two weekly pulses of cyclophosphamide (0.7 g/m2) and 13 plasma exchanges were also given. Antiepileptic treatment was added to the immunosuppressive treatment given the recent general seizures in the context of encephalitis.
Figure 1
Small and non-specific hyperintensities in Magnetic Resonance Imaging (MRI).
Figure 2
Left frontal-temporal cortex hypometabolism and moderate bilateral hippocampic hypometabolism in cerebral positron emission tomography (18FDG-PET).
Catatonia as well as affective and psychotic symptoms progressively improved, but the patient revealed many neurological sequelae. Indeed, she presented with frontal lobe syndrome (perseverations, grasping, lack of emotions, lack of initiative, speech reduction and aphasia), severe impairment of memory, ataxia, stereotyped movements (e.g., chewing movements and teeth grinding), right ptosis and myosis. Early neuropsychological and speech testing confirmed the presence of frontal-like aphasia with perseverations, significant slowness, severe verbal and non-verbal impairment, major memory impairment (in short term and working memory) with confabulations. Furthermore, she was anosognosic. Her cognitive functions were clearly abnormal given her age and school level before this episode (Table1).
Table 1
Course of cognitive assessments after plasma exchange and immunosuppressive treatment
Time
PE ending*
6 months
10 months
14 months
Prednisone (mg per day)
1
0
0
0
Cyclophosphamide (0.7/m2)
2
0
0
0
Plasma exchanges (N received previously)
13
0
0
0
Immunoglobulin (N of cure)
0
3
3
0
WAIS IIIVerbal comprehension index
Similarities
14
17
17
Arithmetic
Impossible
8
8
Vocabulary
7
15
15
Information
8
8
8
13
Comprehension
12
16
16
Working memory index
digit span
1
7
7
Verbal IQ
92
111
111
Perceptual organization index
Matrix reasoning
6
7
11
13
Picture completion Block design matrix
6 1
10 8
10 8
Processing speed index
Symbol search
3
11
11
Digit symbol-coding
10
Refusal
10
Performance IQ
63
100
109
Total IQ
Not valid
107
111
Wechsler Memory (immediate/delayed recall)
Logical memory
2/1
2/6
10/8
Face recognition
2/13
2/13
Verbal paired associates
3/1
3/12
7/12
Family pictures
6/1
6/1
Letter-number sequencing
1
1
7
Spatial span
1
1
PE = Plasma exchange; IQ = Intellectual Quotient; WAIS = Wechsler Adult Intelligence Scale
After the neurological sequelae indicated an encephalopathy with frontal and limbic dysfunction, we evaluated her serum and cerebrospinal fluid for an increase in anti-NMDA-Receptor antibodies. These levels were highly elevated. The anti-NMDA-Receptor encephalitis diagnosis was therefore retained, yet no tumor was found. The patient was transferred to a recovery center, where she received speech therapy and cognitive remediation for her memory loss. Immunosuppressive treatment with intravenous immunoglobulin was prescribed for the next months (Table1), and she continued to improve. Post-cognitive sequelae disappeared within 2 years. Subsequently, she was able to return to school and seemed to have regained her original cognitive abilities (Table1).
Conclusions
In this case report, acute mania with psychotic features deteriorating to catatonic state revealed anti-NMDA-receptor encephalitis. This encephalitis is a multistage illness that progresses from psychosis, memory deficits, seizures, and language disintegration to a state of unresponsiveness with catatonic features [4]. Psychiatric symptoms, including delusions, anxiety, insomnia, and mania, can occur initially, and they usually present less than 2 weeks after prodromal symptoms (headache, fever, nausea, diarrhea or upper respiratory tract symptoms) [4]. The patients are often initially seen by psychiatrists. Anti-NMDA-Receptor encephalitis predominantly affects children and young adults [4,13] and may or may not be associated with a tumor. Approximately 80% of patients are women. The presence of a tumor is more frequent in women who are older than 18 years and who are black [4]. Because of the initial psychiatric presentation, high dosages of antipsychotics were administrated to the patient. Even if the role of antipsychotics is not clear and that catatonic features occur in anti-NMDA-Receptor encephalitis, they may aggravate the catatonic symptoms.
Therapeutic approaches to catatonia are mainly symptomatic. It is recommended to use high dosages of benzodiazepines and to perform electroconvulsive therapy in case of resistance or a life threatening condition [15]. Treatment of the causal organic condition is also warranted. In this case, the patient did not respond to high doses of lorazepam. ECT was discussed but postponed due to signs of acute encephalitis.
A recent literature review showed that organic causes of catatonia in young people make up 20% of all cases [14], and this rate was confirmed in a prospective study [16]. Among the organic causes, encephalitis, caused by infection or immune mechanisms requires specific treatments. In particular, neuropsychiatric systemic lupus erythematosus (SLE) can be revealed by a catatonic syndrome. It is crucial to diagnose and begin an appropriate treatment quickly to improve the patient's prognosis. Plasma exchange appears to be an efficient treatment option in SLE and catatonia, and it avoids the use of ECT [17,18].
In the present case, given the increased antinuclear antibodies, the MRI results (non-specific white matter hyperintensities) and the PET hypometabolism, clinicians first hypothesized the presence of SLE. The presence of antinuclear and/or thyroid peroxidase antibodies, in addition to NMDAR antibodies, has been previously described, most typically in children and can suggest a predisposition to this type of auto immunity [4,13]. Associated plasma exchanges and immunosuppressive therapy were used as treatment. After improvement of the malignant catatonia, neurological markers led to a diagnosis of anti-NMAD-receptor encephalitis, which indicated the need for continuation of immunomodulatory therapy with immunoglobulins. This treatment led to a major improvement in catatonic, psychiatric and neurological symptoms. Management of anti-NMDAR encephalitis is focused on immunotherapy and the detection and removal of a teratoma [4]. Based on an extensive review (400 patients over a 3-year period), Dalmau and colleagues proposed an algorithmic strategy to guide treatment [4]. The first line of immunotherapy consists of corticosteroids, intravenous immunoglobulins, and plasma exchange (alone or in combination). The second line of immunotherapy (rituximab or cyclophosphamide or both) is usually needed in the case of a delayed diagnosis or in the absence of a tumor [4].
Regarding the patient's cognitive impairment, NMDA receptors are known to play a crucial role in synaptic plasticity, which is involved in memory, learning and cognition [19]. Disruption of these receptors can result in seizures and changes in memory, learning and behavior [1]. It is possible to explain the patient's sequelae by a diagnosis of diffuse encephalopathy that is mainly due to frontal and limbic dysfunction. Similarly, an early manifestation with acute severe psychiatric signs and catatonia may be related to dysfunction of the NMDA-R circuitry, as the NMDA-R has been implicated in psychotic symptomatology [20,21].
Interestingly, another case of adolescent catatonia associated with encephalitis has been reported [22]. In that case, encephalitis was paraneoplastic and improved after an ovarian tumor ablation. In retrospect, it is possible that that case also presented was anti-NMDA-receptor encephalitis, given its frequent association with ovarian teratoma [12,13]. Another recent case report showed an excellent recovery after immunotherapy (plasma exchange and corticosteroids) in a case of anti-NMDAR encephalitis in a 12-year-old girl [23].
Recognition of encephalitis by psychiatrists is important because patients may initially present with psychiatric symptoms and catatonic features. Here, symptoms and paraclinical data are in accordance with cases of anti NMDAR encephalitis already reported: severe psychiatric symptoms, seizures, orofacial dyskinesia. In the case of severe and possible life-threatening anti-NMDA-receptor encephalitis, it is essential that a quick and adapted treatment is implemented. Indeed, the prognosis of anti NMDA-R encephalitis varies: 75% of cases recover with immunotherapy and tumor ablation (when present), while 25% of cases lead to severe sequelae and even death [4]. Relapse occurs in 15% of all cases [12].
This case report emphasizes the importance to search for a medical condition in catatonic syndrome of young people to treat and avoid severe neurological sequelae or death. The proposal of the DSM-V workgroup to make catatonia a "specifier" added as a fifth digit to other diagnoses seems likely to reduce rather than enhance clinician awareness of importance of recognizing this syndrome and researching for medical condition, particularly during psychiatric training. By contrast, a large group of experts advocated a unique and broadly-defined code for catatonia as a syndrome, which can be diagnosed acutely in addition to any suspected or established associated disorders [24]. In this case, the initial psychiatric clinical presentation was complicated by a malignant catatonic state, which is now well-described in anti-NMDA-Receptor encephalitis. Child psychiatrists need to know that anti-NMDA-Receptor encephalitis occurs frequently in children and adolescents. Plasma exchanges and immunosuppressive therapy treatments can dramatically improve catatonic syndrome associated with autoimmune dysfunction such as SLE [17,18], PANDAS [25] and NMDA-receptor encephalitis.
Consent statement
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
Declarations
Acknowledgements
This study was funded by theCentre d'Activités et de Recherches en Psychiatrie Infanto-Juvénile(CARPIJ).
In 2009 Susannah Cahalan was a healthy 24-year-old reporter at theNew York Post, one of the country's oldest newspapers, when she suddenly developed a range of worrying symptoms. Her left hand went numb, paranoid thoughts obsessed her mind, and migraines and stomachaches beset her body. Initially diagnosed with mononucleosis, Cahalan continued to grow worse, eventually suffering a series of near-fatal seizures, psychosis, and a gradual loss of brain function. She ended up at New York University's Langone Medical Center, where a team of doctors, led by neurologist Souhel Najjar, diagnosed her with a disease that had been discovered only two years earlier: NMDA-receptor autoimmune encephalitis. In this excerpt Cahalan tells the story of how University of Pennsylvania neuro-oncologist Josep Dalmau first identified the disorder.
Four years earlier, in 2005, Dr. Dalmau had been the senior author on a paper in the neuroscience journalAnnals of Neurologythat focused on four young women who had developed prominent psychiatric symptoms and encephalitis. All had white blood cells in their cerebrospinal fluid, confusion, memory problems, hallucinations, delusions, and difficulty breathing, and they all had tumors called teratomas in their ovaries. But the most remarkable finding was that all four patients had similar antibodies that appeared to be reacting against specific areas of the brain, mainly the hippocampus. Something about the combination of the tumor and the antibodies was making these women very sick.
Dr. Dalmau had noticed a pattern in these four women; now he had to learn more about the antibody itself. He and his research team began to work night and day on an elaborate immunohistrochemistry experiment involving frozen sections of rat brains, which had been sliced into paper-thin pieces and then exposed to the cerebrospinal fluid of those four sick women. The hope was that the antibodies from the cerebrospinal fluid would bind directly to some receptors in the rat brain and reveal a characteristic design. It took eight months of tinkering before a pattern finally emerged.
Dr. Dalmau had prepared the rat brain slides all the same, placing a small amount of cerebrospinal fluid from each of the four patients on each. Twenty-four hours later…[f]our beautiful images, like cave drawings or abstract seashell patterns, revealed the antibodies' binding to the naked eye. "It was a moment of great excitement," Dr. Dalmau later recalled. "Everything had been negative. Now we became totally positive that all four not only had the same illness, but the same antibody."
He had clarified that the pattern of reactivity was more intense in the hippocampus of the rat brain, but this was only the beginning. A far more difficult question now arose: Which receptors were these antibodies targeting? Through a combination of trial and error, plus a few educated guesses about which receptors are most common in the hippocampus, Dr. Dalmau and his colleagues eventually identified the target. Using a kidney cell line bought from a commercial lab that came with no receptors on their surfaces at all, a kind of "blank slate," his lab introduced DNA sequences that direct the cells to make certain types of receptors, allowing the lab to control which receptors were available for binding. Dalmau chose to have them express only NMDA receptors, after figuring out that those were the most likely to have been present in high volume in the hippocampus. Sure enough, the antibodies in the cerebrospinal fluid of the four patients bound to the cells. There was his answer: the culprits were NMDA-receptor-seeking antibodies.
NMDA (N-methyl-D-aspartate acid) receptors are vital to learning, memory, and behavior, and they are a main staple of our brain chemistry. If these are incapacitated, mind and body fail. NMDA receptors are located all over the brain, but the majority are concentrated on neurons in the hippocampus, the brain's primary learning and memory center, and in the frontal lobes, the seat of higher functions and personality. These receptors receive instructions from chemicals called neurotransmitters. All neurotransmitters carry only one of two messages: they can either "excite" a cell, encouraging it to fire an electrical impulse, or "inhibit" a cell, which hinders it from firing. These simple conversations between neurons are at the root of everything we do, from sipping a glass of wine to writing a newspaper lead.
In those unfortunate patients with Dr. Dalmau's anti-NMDA-receptor encephalitis, the antibodies, normally a force for good in the body, had become treasonous persona non grata in the brain. These receptor-seeking antibodies planted their death kiss on the surface of a neuron, handicapping the neuron's receptors, making them unable to send and receive those important chemical signals. Though researchers are far from fully understanding how NMDA receptors (and their corresponding neurons) affect and alter behavior, it's clear that when they are compromised the outcome can be disastrous, even deadly.
Still, a few experiments have offered up some clues as to their importance. Decrease NMDA receptors by, say, 40 percent, and you might get psychosis; decrease them by 70 percent, and you have catatonia. In "knockout mice" without NMDA receptors at all, even the most basic life functions are impossible: most die within ten hours of birth due to respiratory failure. Mice with a very small number of NMDA receptors don't learn to suckle, and they simply starve to death within a day or so. Those mice with at least 5 percent of their NMDA receptors intact survive, but exhibit abnormal behavior and strange social and sexual interactions. Mice with half their receptors in working order also live, but they show memory deficits and abnormal social relationships.
As a result of this additional research, in 2007, Dr. Dalmau and his colleagues presented another paper, now introducing his new class of NMDA-receptor-seeking diseases to the world. This second article identified twelve women with the same profile of neurological symptoms, which could now be called a syndrome. They all had teratomas, and almost all of them were young women. Within a year after publication, one hundred more patients had been diagnosed; not all of them had ovarian teratomas and not all of them were young women (some were men and many were children), enabling Dr. Dalmau to do an even more thorough study on the newly discovered, but nameless, disease.
"Why not name it the Dalmau disease?" people often asked him. But he didn't think "Dalmau disease" sounded right, and it was no longer customary to name a disease after its discoverer. "I didn't think that would be wise. It's not very humble." He shrugged.
By the time I was a patient at NYU, Dr. Dalmau had fine-tuned his approach, designing two tests that could swiftly and accurately diagnose the disease. As soon as he received my samples, he could test the spinal fluid. If he found that I had anti-NMDA-receptor autoimmune encephalitis, it would make me the 217th person worldwide to be diagnosed since 2007. It just begged the question: If it took so long for one of the best hospitals in the world to get to this step, how many other people were going untreated, diagnosed with a mental illness or condemned to a life in a nursing home or a psychiatric ward?
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According to old Chinese advice, it is wise never to discuss politics or religion even amongst best friends. Religious belief can often blur judgment in the wisest of people.
Thirty years ago, a patient of mine was unconscious for 23 days and it was mother's belief that it was through prayer that her daughter was saved. I did not argue with her then.
But perhaps God works through his people in his own way. Discoveries in Medicine should therefore enhance our faith rather than the other way round.
It took nearly 30 years for the real answer to her prayers to really emerge.
I was staying at our resort in Boquete and was having dinner with three friends all of them with medical connections. One was in hospital administration and one a nurse. The husband of the nurse was a pharmacist. Somehow the conversation drifted into medical topics and knowing that I am a Child Psychiatrist the pharmacist started talking about his nephew who was nearly sent to a mental institution as he suffers from catatonia and doctors eventually diagnosed schizophrenia and put him on antipsychotics. Luckily the catatonic symptom probably saved him as some bright young thing just read the book Brain On Fire and gave him the Clock Test. That led to the NMDAR antibody testing that proved positive. He responded well to the treatment regime that has been developed and is off all antipsychotic medication.
My Teratoma patient was lucky as she belong to that group that improved without further treatment once the Teratoma was removed. She eventually had a baby.
NEW ORLEANS — A mysterious, difficult-to-diagnose, and potentially deadly disease that was only recently discovered can be controlled most effectively if treatment is started within the first month that symptoms occur, according to a new report by researchers from the Perelman School of Medicine at the University of Pennsylvania. The researchers analyzed 565 cases of this recently discovered paraneoplastic condition, called Anti-NMDA Receptor Encephalitis, and determined that if initial treatments fail, second-line therapy significantly improves outcomes compared with repeating treatments or no additional treatments (76 percent versus 55 percent). The research is being presented at theAmerican Academy of Neurology's 64th Annual Meeting in New Orleans.
565 cases! Not so rare!
The condition occurs most frequently in women (81 percent of cases), and predominately in younger people (36 percent of cases occurring in people under 18 years of age, the average age is 19). Symptoms range from psychiatric symptoms, memory issues, speech disorders, seizures, involuntary movements, to decreased levels of consciousness and breathing. Within the first month, movement disorders were more frequent in children, while memory problems and decreased breathing predominated in adults.
My patient was under 18 and presented with catatonia symptoms. She later lose consciousness and was ventilated.
"Our study establishes the first treatment guidelines for NMDA-receptor encephalitis, based on data from a large group of patients, experience using different types of treatment, and extensive long-term follow-up," said lead authorMaarten Titulaer, MD, PhD, clinical research fellow in Neuro-oncology and Immunology in the PerelmanSchool of Medicine at the University of Pennsylvania. "In addition, the study provides an important update on the spectrum of symptoms, frequency of tumor association, and the need of prolonged rehabilitation in which multidisciplinary teams including neurologists, pediatricians, psychiatrists, behavioral rehabilitation, and others, should be involved."
The disease was first characterized by Penn'sJosep Dalmau, MD, PhD, adjunct professor of Neurology, andDavid R. Lynch, MD, PhD, associate professor of Neurology and Pediatrics, in Annals of Neurology in 2007. One year later, the same investigators in collaboration withRita Balice-Gordon, PhD, professor of Neuroscience, characterized the main syndrome and provided preliminary evidence that the antibodies have a pathogenic effect on the NR1 subunit of the NMDA receptor in theLancet Neurology in December 2008. The disease can be diagnosed using a test developed at the University of Pennsylvania and currently available worldwide. With appropriate treatment, almost 80 percent of patients improve well and, with a recovery process that may take many months and years, can fully recover.
Teratoma: finally!
In earlier reports, 59 percent of patients had tumors, most commonly ovarian teratoma, but in the latest update, 54 percent of women over 12 years had tumors, and only six percent of girls under 12 years old had ovarian teratomas. In addition, relapses were noted in 13 percent of patients, 78 percent of the relapses occurred in patients without teratomas.
As Anti-NMDA Receptor Encephalitis, the most common and best characterized antibody-mediated encephalitis, becomes better understood, quicker diagnosis and early treatment can improve outcomes for this severe disease.
The study was presented in a plenary session on Wednesday, April 25, 2012 ET at 9:35 AM at the American Academy of Neurology's annual meeting.
[PL01.001] Clinical Features, Treatment, and Outcome of 500 Patients with Anti-NMDA Receptor Encephalitis
Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies Of 100 patients with anti-NMDA-receptor encephalitis, a disorder that associates with antibodies against the NR1 subunit of the receptor, many were initially seen by psychiatrists or admitted to psychiatric centres but subsequently developed seizures, decline of consciousness, and complex symptoms requiring multidisciplinary care. While poorly responsive or in a catatonic-like state, 93 patients developed hypoventilation, autonomic imbalance, or abnormal movements, all overlapping in 52 patients. 59% of patients had a tumour, most commonly ovarian teratoma. Despite the severity of the disorder, 75 patients recovered and 25 had severe deficits or died. Related paper:
The following is extracted from The Cockroach Catcher: Chapter 29 The Power of Prayers.
According to old Chinese advice, it is wise never to discuss politics or religion even amongst best friends.
Religious belief can often blur judgement in the wisest of people. In psychiatry it is sometimes not easy. This is particularly true in cases of florid psychosis, which often presents with symptoms of hallucination, delusion and even vision.
I remember my early days of psychiatry in a mental hospital in Hong Kong. Yes, it was the days of 2000-bed hospitals. Yes, it was the days of Medical Superintendents who had supreme power and all doctors of whatever rank and experience were Mental Health Officers with special authority to sign papers for compulsory admissions. The forensic unit was contained within the same complex. Those were the days when we encountered psychosis in the raw so to speak. All the colony’s really mad people were admitted to this one place set in the furthest corner of the colony. In our year seven of us decided without much discussion that we all wanted to go into psychiatry. That was over 10% and all had quite idealistic reasons. It was perhaps a bit of a disappointment to our parents that we did not pursue a more conventional specialty that might provide us with more status and financial reward. Then there was the fear of contamination that somehow one might become mad too. Recent day medical students are said to shy away from psychiatry for these same reasons. Education seems to have little effect on superstition. ......................................….read the full Chapter: HERE
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