Sethiya et al presented a constellation of solid neurological signs
in a middle-aged male.
1. The author did not add a differential diagnosis list for this
constellation?
2. The MRI images do not "teach" anything. The right image is an
axial T2 FLAIR one while the left image is a sagittal T2-weighted one.
Hyper- or hypo-intense signals in the mesencephalon on these films; the
p...
Sethiya et al presented a constellation of solid neurological signs
in a middle-aged male.
1. The author did not add a differential diagnosis list for this
constellation?
2. The MRI images do not "teach" anything. The right image is an
axial T2 FLAIR one while the left image is a sagittal T2-weighted one.
Hyper- or hypo-intense signals in the mesencephalon on these films; the
potential cause(s) of this imaging abnormality? In addtion, there is a
striking C-shaped hyper-intense signal around the Sylvian aqueduct on the
FLAIR film. What are these, the readership might ask?
3. The autopsy addressed the lung as the cause of death; the
patient's brain undiagnosed disaster was ignored?
4. The case was published sometime ago in the website and the legend
for figure one was "corrected." I think the journal should mention that
there is an "erratum;" I have "2 PDFs" of his article!
So, after all, it's all about "Images In." As a neurologist who is
interested in teaching under- and postgraduates, I may ask: What have we
learned from this case's "images?"
Thanks!
Conflict of Interest:
None declared
Editor's Note - there was indeed a previous version of this article that contained significant errors so a correct version was published. We agree this should have been more transparent to the readers and a notice will be published shortly notifying readers to the previous publication
Yes, brain regression is known in certain infiltrative and
degenerative conditions, but, the problem as raised by Prof Agrawal S and
Nathani S here is, that Ursula von Schenk et al from Germany, when first
reported brain regression due to B12 deficiency followed by recovery
shortly on therapy, it contradicted the very concept of atrophy and
regression. And to the non radio/imaging experts it appeared simply that
two ima...
Yes, brain regression is known in certain infiltrative and
degenerative conditions, but, the problem as raised by Prof Agrawal S and
Nathani S here is, that Ursula von Schenk et al from Germany, when first
reported brain regression due to B12 deficiency followed by recovery
shortly on therapy, it contradicted the very concept of atrophy and
regression. And to the non radio/imaging experts it appeared simply that
two images at different planes were used to claim high signal image
pathology in their figure 1. Zekai Avci et al from Turkey 2003 presented
good images for the same claim, yet, to the non image experts there were
no visible fronto-parietal hyper intensive lesions appreciable in cortex.
It looked as if gray matter image was seen in the fist figure and white
with gray in second with no appreciable intensity differences. These
researches of course in the domain of Radio and Imaging, experts could be better interpretors. In the present case, since Agarwal and
Naithani pointed out, it appears that their opinion is scientifically
factual.
Schistosoma mansoni parasitizes medium sized mesenteric veins and
arteries and its ovum is armed with a lateral spine, so intestinal mucosa
suffers on account of ova from mesenteric arteries reaching the mucosal
capillaries. Spine helps rupture of capillary facilitating release of the
ovum and blood into the lumen of the intestine. So diarrhoea in case of S
mansoni infestation is often blood mixed, particularly in the ph...
Schistosoma mansoni parasitizes medium sized mesenteric veins and
arteries and its ovum is armed with a lateral spine, so intestinal mucosa
suffers on account of ova from mesenteric arteries reaching the mucosal
capillaries. Spine helps rupture of capillary facilitating release of the
ovum and blood into the lumen of the intestine. So diarrhoea in case of S
mansoni infestation is often blood mixed, particularly in the phase when
ova are detectable in the stool. Authors while correctly pointed out
currently low incidence of this disease in European countries, image of
the ovum of S mansoni under microscope in this case should have been shown
for sake of the young generation of diagnosticians in the region.
On 24 April 2010 at about 8 pm I was taken to Accident and Emergency
Department of Prince of Wales hospital (Sydney) by my daughter because I
could not recall what had happened during the afternoon. I could remember
events up till meeting friends for lunch at 12 noon, then events from 5 pm. My
daughter stated that I "was not myself" and repeated same
questions/phrases since I returned home at 4:30 pm,
On 24 April 2010 at about 8 pm I was taken to Accident and Emergency
Department of Prince of Wales hospital (Sydney) by my daughter because I
could not recall what had happened during the afternoon. I could remember
events up till meeting friends for lunch at 12 noon, then events from 5 pm. My
daughter stated that I "was not myself" and repeated same
questions/phrases since I returned home at 4:30 pm,
I do not have any history of migraine headache, epilepsy nor head
injury. The following investigations were taken during my 11 hours stay at
the hospital: ECG (sinus rhythm); CT Brain (nil acute bleed or mass); FBC (normal).
I started to fully orientate about 1 am and was discharged at 8:30 am the
following morning. My diagnosis Transient Global Amnesia.
I found this article about TGA associated with statin; I wonder if my
episode was caused by statin. I was put on 5 mg of rosuvastatin 10 days
prior to my amnesia.
B12 deficiency has always been a puzzle in pediatric population.
Theoretically B12 deficiency is claimed to not occur in children due to
reduced need of children and it takes years to develop cobalamine
deficiency in children from malnutrition.
Although most B12 deficient infants are failing to thrive, the aetiology
for B12 deficiency is probably intrauterine and may be maternal B12
deficiency in addition, which explain...
B12 deficiency has always been a puzzle in pediatric population.
Theoretically B12 deficiency is claimed to not occur in children due to
reduced need of children and it takes years to develop cobalamine
deficiency in children from malnutrition.
Although most B12 deficient infants are failing to thrive, the aetiology
for B12 deficiency is probably intrauterine and may be maternal B12
deficiency in addition, which explains age of onset of B12 deficieny
symptoms in children from age 8 month onwards.
In India, we come across various manifestations of B12 deficiency apart
from anemia. Rather anemia is the least common manifestation of B12
deficiency in children. This is due to the fact that dietary and breast
milk folate can partially reverse the hematological symptoms. Also
idiopathic bone marrow suppression with thrombocytopenia or leucopenia may
be associated with macrocytosis with anemia.
So most infants purely manifest as neurological syndromes.
Various mechanisms of actions of B12 or cyanocobalamin in DNA synthesis
and myelin formation nay explain various manifestations in children.
Sensory symptoms of peripheral neuropathy being difficult to test in
infants, they manifest as lethargy, apathy and depressed reflexes which
may be likely to be interpreted as neuroregression.
Central nervous symptoms have been documented in literature from lethargy
or convulsion to coma and mental retardation. However, tremors are the
most often seen neurological symptoms in infants as described in infantile
tremor syndrome.
Reversible hyperpigmentation of skin especially over digits and toes has
been often associated with B12 deficiency. It may be a common accompanying
feature in infantile tremor syndrome.
It is interesting to label these neurological features as neurorgression
solely due to neuroimaging evidence.
RDD is a rare histiocytic proliferative disorder of unknown etiology,
commonly presents with painless massive lymphadenopathy and multiple extra
nodal manifestations. Here we present a 13-yr old girl who presented with
irregular low-grade fever with malaise, anorexia and nausea for last six
months followed by five painless soft tissue swellings over the scalp,
4X3cm in diameter without bony involvement and multiple bilater...
RDD is a rare histiocytic proliferative disorder of unknown etiology,
commonly presents with painless massive lymphadenopathy and multiple extra
nodal manifestations. Here we present a 13-yr old girl who presented with
irregular low-grade fever with malaise, anorexia and nausea for last six
months followed by five painless soft tissue swellings over the scalp,
4X3cm in diameter without bony involvement and multiple bilateral painless
cervical & submandibular lymph nodes, 2-3 cm in diameter and
progressive eyelid swelling and protrusion of eyeballs since last 20 days.
Isthmus and left lobe of thyroid gland were moderately enlarged and non-
tender. She also had mediastinal lymphadenopathy compressing the left main
broncus and have dry irritating cough and progressive exertional shortness
of breath since last 15 days with severe dyspnoea and stridor on the day
of admission. There were no history of haemoptysis, weight loss,
arthralgia, rashes, photophobia, bleeding manifestations, high-risk sexual
behavior, or contact with animals. Her thyroid function was normal and anti-TPO antibody was negative.
Fine needle aspiration was done from thyroid gland, scalp mass and
cervical lymph node and was sufficient to diagnose to be a case of Rosai
Dorfman Disease.
Thyroid involvement in RDD is a rare entity and commonly occurs in
older women (mean age 56.3 years) whereas nodal RDD predominantly
presents in early age.[1] Our patient presented at 13 years of age without
any thyroid dysfunction and recovered fully with short course of
prednisolone therapy.
Reference
1. Lee FY, Jan YJ, Chou G, Wang J, Wang CC. Thyroid involvement in
Rosai-Dorfman disease. Thyroid 2007;17:471-6.
The evidence presented by authors (Brian Hurwitz,and Joshua
Richardson) is informative. However, it may be added further that Long-haul
air travel has been well known to give rise to high altitude motion
sickness, cerebellar edema and speech and orientation problems[1]. The
young 14-year-old fellow and his father, since, showed no investigative
findings confirmatory of viral disease. So it could be that they were more
sus...
The evidence presented by authors (Brian Hurwitz,and Joshua
Richardson) is informative. However, it may be added further that Long-haul
air travel has been well known to give rise to high altitude motion
sickness, cerebellar edema and speech and orientation problems[1]. The
young 14-year-old fellow and his father, since, showed no investigative
findings confirmatory of viral disease. So it could be that they were more
susceptible to air travel disease than the fellow passengers, hence,
required a careful MRI brain to exclude anything which could likely
facilitate edema or hypoxia of the brain more than usual.
References:
1. Cesarone MR et al. Prevention of Edema in Long Flights with Pycnogenol. Clin.Appl.Thromb.Hemost. 2005;11(3):289-294.
Sir,caption marks which appear missed on MRI images in this case are important for learning of the new and the practicing generations of the pathologists besides of the imaging diagnosticians, and clinicians. For the pathologists MRI images give cut surface views in vivo helpful in final diagnosis on biopsy or autopsy where ever required. Image markings hence may be promoted by reviewers and editors.
Sir,caption marks which appear missed on MRI images in this case are important for learning of the new and the practicing generations of the pathologists besides of the imaging diagnosticians, and clinicians. For the pathologists MRI images give cut surface views in vivo helpful in final diagnosis on biopsy or autopsy where ever required. Image markings hence may be promoted by reviewers and editors.
We are thankful to Epstein and Naqvi for reporting this case and
reminding us of its lesson. However, I would like to address the
following:
The cerebellum is supplied by three arteries; posterior inferior
cerebellar arteries (PICA), anterior inferior cerebellar artery AICA)
which is usually a single artery, and superior cerebellar arteries (SCA).
These vessels and their branches anastomose with each other to f...
We are thankful to Epstein and Naqvi for reporting this case and
reminding us of its lesson. However, I would like to address the
following:
The cerebellum is supplied by three arteries; posterior inferior
cerebellar arteries (PICA), anterior inferior cerebellar artery AICA)
which is usually a single artery, and superior cerebellar arteries (SCA).
These vessels and their branches anastomose with each other to form a very
rich vascular network. In situ thrombosis or an embolic material may
occlude any of these arteries ending with infarction of the cerebellum.
The resulting clinical manifestations are due to the damaged vascular
territory and the status of the collaterals.
According to Barth [1] and Toghi [2], we may face of one of four
topographic syndromes of cerebellar infarctions depending on the artery
involved:
1. The PICA syndrome (40%).
2. The SCA syndrome (35%).
3. A watershed superficial cortical and deep parenchymal syndrome (20%).
4. The AICA occlusion syndrome constitutes 5% of cases only.
Practically, the above syndromes are further categorized as
cerebellar infarction with secondary fourth ventricle and brainstem
compressions or cerebellar infarction without fourth ventricle and
brainstem compressions.
Another problem with such infarcts is the herniation syndromes. This
massive edematous and infracted cerebellar tissue may force the rest of
the cerebellum to herniate up (transtentorial herniation) or downward
(conning).
This non-contrast brain CT scan is consistent with SCA occlusion. The
infracted area is relatively large. Such large and edematous infarctions
can result in secondary compression of the fourth ventricle and Sylvius
aqueduct producing acute obstructive hydrocephalus. The progressive
obtundation of this patient can be ascribed to both, the brainstem
compression and acute obstructive hydrocephalus [3,4]. However, the degree
of the hydrocephalus is not that severe and cannot explain such a sudden
fall in the consciousness level. I think the brainstem compression was the
main culprit here.
However, one must emphasize that brainstem compression and acute
obstructive hydrocephalus complicate only 7% of SCA occlusion syndromes
(although the infarcted area is relatively large) and that this artery is
most likely blocked by a cardiac source of embolism [5].
Amarenco and Hauw in 1990 [6] found that large ischemic cerebellar
infarctions tend to occur in the territory of the SCA; their main
observation was the alteration in the level of consciousness, which can
occur hours or even days after the vascular insult. One year later,
Amarenco [3] demonstrated that an emergency surgery (with posterior fossa
decompression or ventriculostomy or both) is often required to save the
life of these patients. In addition, Chen and coworkers [7] found that
this intervention is not only life-saving, but the long-term prognosis is
very good after surgery in terms of functional dependence and quality of
life; there was no mortality in their series. However, Ogasawara et al [8]
noticed that the prognosis after surgical intervention for massive
cerebellar edema of ischemic infarctions depends mainly on the pre-
surgical co-existent brainstem infarction.
Finally yet importantly, it is well-known that cerebellar lesions
result in unilateral signs; the patient demonstrated left-sided
incoordination. The author was very brief in describing the neurological
findings of the patient after the deterioration in the level of
consciousness, and he has not provided us a short paragraph about the
brain CT signs of early hydrocephalus. In addition, the author has not
mentioned in the text that the hydrocephalus is an acute one and is
obstructive; although we can conclude this from the overall scenario, but
for the readership, this should be included in the text. However,
reference number one mentioned acute hydrocephalus.
References:
1. Barth A, Bogousslavsky J, Regli F. The clinical and topographic
spectrum of cerebellar infarcts: a clini-cal-magnetic resonance imaging
correlation study. Ann Neurol 1993;33:451-56.
2. Tohgi H, Takahashi S, Chiba K, et al. Cerebellar infarction.
Clinical and neuroimaging analysis in 293 patients. Stroke 1993;24:1697-
1701.
3. Amarenco P. The spectrum of cerebellar infarctions. Neurology
1991;41:973-79.
5. Kase CS, Norrving B, Levine SR, et al. Cerebellar infarction.
Clinical and anatomic observations in 66 cases. Stroke 1993;24:76-83.
6. Amarenco P, Hauw JJ. Cerebellar infarction in the territory of the
superior cerebellar artery: a clinicopathologic study of 33 cases.
Neurology 1990b;40:1383-1390.
7. Chen HJ, Lee TC, Wei CP. Treatment of cerebellar infarction by
decompressive suboccipital craniectomy. Stroke 1992 Jul;23(7):957-61.
8. Ogasawara K, Koshu K, Nagamine Y, Fujiwara S, Mizoi K, Yoshimoto
T. Surgical decompression for massive cerebellar infarction. No Shinkei
Geka 1995 Jan;23(1):43-8.
Catatonia is not a diagnosis. Rather, catatonia is a descriptive term
for a presentation observed in a wide variety of disorders. Catatonia
continues to be recognised in the UK by about 1/3 of psychiatrists
surveyed in South West England and Wales. The understanding of the
condition may differ. This implies that under diagnosis may lead to
suboptimal treatment and fatalities as the differential diagnosis of
catatonia in...
Catatonia is not a diagnosis. Rather, catatonia is a descriptive term
for a presentation observed in a wide variety of disorders. Catatonia
continues to be recognised in the UK by about 1/3 of psychiatrists
surveyed in South West England and Wales. The understanding of the
condition may differ. This implies that under diagnosis may lead to
suboptimal treatment and fatalities as the differential diagnosis of
catatonia includes lethal forms such as neuroleptic malignant syndrome and
malignant hyperpyrexia which are made worse by antipsychotics. The exact
cause of catatonia has not been elucidated, but a number of hypotheses
have been offered.
According to Northoff (2002), a 'top-down modulation'
of basal ganglia due to deficiency of cortical gamma-aminobutyric acid
(GABA), the primary inhibitory neurotransmitter of the brain, may explain
the motor symptoms of catatonia. This explanation might account for the
dramatic therapeutic effect of benzodiazepines, which cause an increase in
GABA activity. Similarly, hyperactivity of glutamate, the primary
excitatory neurotransmitter, has also been suggested as an underlying
neurochemical dysfunction.
Researchers have suggested that catatonia is
caused by a sudden and massive blockade of dopamine. This may explain why
dopamine-blocking antipsychotics are not generally beneficial in
catatonia. Indeed, by exacerbating dopamine deficiency, antipsychotics may
actually precipitate a worsening of the condition. Positron emission
tomography (PET) has identified abnormalities in metabolism bilaterally in
the thalamus and frontal lobes.
Kahlbaum in 1874 originally described
catatonia as being a syndrome characterised by unusual motor symptoms but
it was incorporated into the subtypes of schizophrenia in the 20th century. It has now been recognised that classification should better reflect
that catatonia occurs in many illnesses(Taylor et al 2003). In the early
1970s it was suggested that catatonia was disappearing however there were
no standardised diagnostic instruments such as the Bush Francis Catatonia
Rating Scale (BFCRS).
Catatonia is a syndrome that encompasses more than
two dozen signs, some of which are relatively non-specific. The catatonic signs are listed as follows: Ambitendency, Automatic, Obedience, Aversion, Catalepsy, Echolalia, Echopraxiam, Excitement, Forced, Grasping, Gegenhalten, Grimacing, Immobility, Logorrhoea, Mannerisms, Mitgehen, Mitmachen, Mutism, Negativism, Perseveration, Posturing, Psychological pillow, Rigidity, Staring, Stereotypies, Stupor, Verbigeration, Waxy flexibility and Withdrawal.
Prevalence rates have changed from 20-30% to 2-10% over the last century,
but have not changed in the last 30 years . Prevalence was reported as 7.6
- 38% by Taylor et al who collected worldwide data on catatonia on
hospitalised patients from 1920 to 2000. The current frequency of
catatonia in international populations is unknown. The few epidemiological
studies report vastly different rates. These suggest that the occurrence
of catatonia may differ greatly from one location to another. On the other
hand, studies suggest that many cases of catatonia may be undiagnosed
Differential diagnoses of catatonia: Schizophrenia, Depression,
Mania, Organic disorders, eg, infections, epilepsy, metabolic disorders,
Drugs (prescribed or recreational), Hysteria (psychogenic catatonia) and
Idiopathic. Some 40 or more phenomena identify catatonia but only 2
prominent signs for several to 24 hours are sufficient for diagnosis.
Taylor et al have more recently proposed a classification scheme dividing
catatonia into (i)non-malignant (Kahlbaum syndrome) treated with lorazepam
6-20 mg/day, (ii) delirious catatonia (delirious mania, excited catatonia)
treated with high dose lorazepam or ECT and, (iii) malignant catatonia
(neuroleptic malignant syndrome, serotonin syndrome) treated by life support. Others believes that catatonia should be classified as an
independent syndrome with the following subtypes: non-malignant, delirious
and malignant. A further classification, used by the Wernicke-Kleist-
Leonhard school of psychiatry, identifies two main types of catatonia -
systematic and periodic. These appear to have significant differences in
symptomatology, treatment and prognosis. The systematic type is less
genetically determined, has a higher prevalence and earlier age at onset
in males, and is associated with mid-gestational infections. Periodic
catatonia has no differences in either age at onset or prevalence between
males and females and it was confirmed genetic linkage, the susceptibility
site being 15q15. Catatonic patients will need a comprehensive physical
examination, with specific emphasis on neurological signs, and a thorough
mental state examination, with special emphasis on identifying catatonic
signs. This, coupled with the history, usually provided by an informant,
may give a clue as to whether the catatonia is functional or organic, and
will also determine whether the patient needs admission to a medical or a
psychiatric ward. Although catatonia occurs in both functional and organic
disorders, the treatment of the catatonic phase is essentially the same,
and most patients respond well to benzodiazepines or ECT. In some cases,
treatment of the underlying disorder may have to be suspended (e.g. not
using antipsychotics in acute catatonic schizophrenia) until the catatonic
phase is resolved. This suggests that catatonia is a unique syndrome that
requires treatment in its own right, independent of any underlying
disorder.
Treatments that have a strong evidence base (Benzodiazepines and
Electroconvulsive therapy). Other options (usually reserved for catatonia
resistant to benzodiazepines and ECT) Mood stabilisers: especially
carbamazepine, Antipsychotics, NMDA antagonists: amantadine and memantine
Dopamine agonists (e.g. bromocriptine) and skeletal muscle relaxants (e.g.
dantrolene), especially if neuroleptic malignant syndrome is suspected.
Obviously, if a patient with catatonia does not eat or drink for prolonged
periods this will lead to dehydration and its attendant complications. The
immobility of catatonia may increase the risk of deep-vein thrombosis.
Researchers have highlighted the increased risk of death due to pulmonary
embolism in patients with persistent catatonia; such deaths occurred only
after the second week of catatonia, often without warning. During the
phase of catatonic excitement, the patient may pose a significant risk of
harm to self and others.
Catatonia continues to be recognised, but the
understanding of the condition differs which could result in under
diagnosis and suboptimal treatment. The use of rating scales may ensure
more cases are identified. There is a need to raise awareness amongst
clinicians of this often forgotten entity.
References
Bush G, Fink M, Petrides G, Dowling F, Francis A. (1996) Catatonia .I. Rating Scale and standardised examination. Acta
Psychiatrica. Scandinavica. 93(2) :129-136.
Chalasani P, Healey D, Morriss R. (2005) Presentation and frequency of catatonia in new
admissions to two acute psychiatric admission units in India and Wales.
Psychological Medicine , 35, 1667- 1675
Dear Editor,
Sethiya et al presented a constellation of solid neurological signs in a middle-aged male.
1. The author did not add a differential diagnosis list for this constellation?
2. The MRI images do not "teach" anything. The right image is an axial T2 FLAIR one while the left image is a sagittal T2-weighted one. Hyper- or hypo-intense signals in the mesencephalon on these films; the p...
Yes, brain regression is known in certain infiltrative and degenerative conditions, but, the problem as raised by Prof Agrawal S and Nathani S here is, that Ursula von Schenk et al from Germany, when first reported brain regression due to B12 deficiency followed by recovery shortly on therapy, it contradicted the very concept of atrophy and regression. And to the non radio/imaging experts it appeared simply that two ima...
Schistosoma mansoni parasitizes medium sized mesenteric veins and arteries and its ovum is armed with a lateral spine, so intestinal mucosa suffers on account of ova from mesenteric arteries reaching the mucosal capillaries. Spine helps rupture of capillary facilitating release of the ovum and blood into the lumen of the intestine. So diarrhoea in case of S mansoni infestation is often blood mixed, particularly in the ph...
On 24 April 2010 at about 8 pm I was taken to Accident and Emergency Department of Prince of Wales hospital (Sydney) by my daughter because I could not recall what had happened during the afternoon. I could remember events up till meeting friends for lunch at 12 noon, then events from 5 pm. My daughter stated that I "was not myself" and repeated same questions/phrases since I returned home at 4:30 pm,
I do not h...
B12 deficiency has always been a puzzle in pediatric population. Theoretically B12 deficiency is claimed to not occur in children due to reduced need of children and it takes years to develop cobalamine deficiency in children from malnutrition. Although most B12 deficient infants are failing to thrive, the aetiology for B12 deficiency is probably intrauterine and may be maternal B12 deficiency in addition, which explain...
RDD is a rare histiocytic proliferative disorder of unknown etiology, commonly presents with painless massive lymphadenopathy and multiple extra nodal manifestations. Here we present a 13-yr old girl who presented with irregular low-grade fever with malaise, anorexia and nausea for last six months followed by five painless soft tissue swellings over the scalp, 4X3cm in diameter without bony involvement and multiple bilater...
The evidence presented by authors (Brian Hurwitz,and Joshua Richardson) is informative. However, it may be added further that Long-haul air travel has been well known to give rise to high altitude motion sickness, cerebellar edema and speech and orientation problems[1]. The young 14-year-old fellow and his father, since, showed no investigative findings confirmatory of viral disease. So it could be that they were more sus...
Conflict of Interest:
...We are thankful to Epstein and Naqvi for reporting this case and reminding us of its lesson. However, I would like to address the following:
The cerebellum is supplied by three arteries; posterior inferior cerebellar arteries (PICA), anterior inferior cerebellar artery AICA) which is usually a single artery, and superior cerebellar arteries (SCA). These vessels and their branches anastomose with each other to f...
Catatonia is not a diagnosis. Rather, catatonia is a descriptive term for a presentation observed in a wide variety of disorders. Catatonia continues to be recognised in the UK by about 1/3 of psychiatrists surveyed in South West England and Wales. The understanding of the condition may differ. This implies that under diagnosis may lead to suboptimal treatment and fatalities as the differential diagnosis of catatonia in...
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