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
MRI in this case depicted tumor in a location where carcinoma is the most
common neoplasm and lymphoma rare. Evidence is hardly of any use for
readers unless microscopic evidence accompanied the MRI images. More
important it was in view of the documentation that it was not typical
lymphoid lesion in biopsy report but a lymphoepithelial mass; so, not
necessarily neoplasm nor necessarily lymphoma, hence, awaiting final
di...
MRI in this case depicted tumor in a location where carcinoma is the most
common neoplasm and lymphoma rare. Evidence is hardly of any use for
readers unless microscopic evidence accompanied the MRI images. More
important it was in view of the documentation that it was not typical
lymphoid lesion in biopsy report but a lymphoepithelial mass; so, not
necessarily neoplasm nor necessarily lymphoma, hence, awaiting final
diagnosis.
I read with interest this article about intra-cranial dural venous sinus thrombosis, and many
thanks go to the authors for the images.
Because the article is an "Images in...," I have the following
notes:
The images do not tell which dural sinus (or sinuses) is
thrombosed.
Pointing out to the abnormal areas on the images would be very
helpful to the readership.
Brief notes about the "empty delta sign" is very important, I
believe.[1]
Figure 3 demonstrates a coronal section of the brain, not a sagittal one. Where is the empty delta sign? The white triangular area
at the top of the image or the one at the left side?
1. Virapongse C, Cazenave C, Quisling R, Sarwar M, Hunter S. The
empty delta sign: frequency and significance in 76 cases of dural sinus
thrombosis. Radiology 1987;162:779-785.
Very significant cases of para neoplastic syndrome are described by
authors, but, images of the tumors claimed to be the cause of the disease
should have been shown for awareness of the reader experts of Medical
Science for future utility to the benefit of the patients.
Here is a very good case of delayed contact dermatitis due to a known
cosmetic allergen called Henna and hence this paper is also of public health significance. Allergen did take few days to precipitate
allergic manifestations with dermatitis and eruptions which authors
noticed to be infected and giving rise to scar formation which appeared
like keloid due to oedema or hypertrophy. These changes, however, do not
qualify...
Here is a very good case of delayed contact dermatitis due to a known
cosmetic allergen called Henna and hence this paper is also of public health significance. Allergen did take few days to precipitate
allergic manifestations with dermatitis and eruptions which authors
noticed to be infected and giving rise to scar formation which appeared
like keloid due to oedema or hypertrophy. These changes, however, do not
qualify the lesion to be delayed hypersensitivity type IV. That would
require biopsy to show presence of macrophages and granulomas. To mix up
delayed allergic dermatitis with delayed hypersensitivity type IV and to
it with Keloid does not appeal that too without any histopathological
evidence.
Co-occurrence of psychosis and multiple sclerosis is uncommon. Most
reports of psychoses and multiple sclerosis are single case studies.
Literature review identified 39 case reports, a number that does not
exceed chance expectation. This demonstrated that people with multiple
sclerosis and psychosis are more likely to have plaques involving the
temporal horns bilaterally.
Co-occurrence of psychosis and multiple sclerosis is uncommon. Most
reports of psychoses and multiple sclerosis are single case studies.
Literature review identified 39 case reports, a number that does not
exceed chance expectation. This demonstrated that people with multiple
sclerosis and psychosis are more likely to have plaques involving the
temporal horns bilaterally.
Some studies suggested that psychosis in
multiple sclerosis is distinct from schizophrenia as it has a later age at
onset, quicker resolution, fewer relapses, better response to treatment
and a better prognosis.
According to McDonald criteria, multiple
sclerosis is a condition in which the CNS of a person present a special
kind of distributed lesions. Therefore the only proved diagnosis of MS can
be made upon autopsy, or occasionally upon biopsy, where lesions typical
of MS can be directly detected through standard histopathological
techniques. The pathophysiology of those multiple scars (sclerosis) is
complex. At least five characteristics are present in CNS tissues of MS
patients: inflammation beyond classical white matter lesions; intrathecal
Ig production with oligoclonal bands; an environment fostering immune cell
persistence; follicle-like aggregates in the meninges and a disruption of
the blood-brain barrier also outside of active lesions. Apart from the
usually known white matter demyelination, also the cortex and deep gray
matter (GM) nuclei are affected, together with diffuse injury of the
normal-appearing white matter. There are three regions: intra cortical,
mixed gray-white matter, and juxta cortical.
Demyelinations are more
frequent in men than in women, and they can partly explain cognitive
deficits. In general behavioural and affective disturbances accompany
multiple sclerosis but are also seen in other inflammatory demyelination
diseases of the CNS. Incidence of some psychic manifestations in
demyelinating diseases of the CNS clearly shows relationship with
intensity and localization of demyelinating lesions. One of the most
prominent psychic changes, depression, often precedes relapses and shows
regression in remission period. It is also more common in patients with MS
than in patients with other neurological diseases. There are no data for
the prevalence of psychosis in other demyelinating diseases. On rare
occasion pure psychiatric symptoms are the first manifestation of multiple
sclerosis or acute disseminated encephalomyelitis.
Given the current media
descriptions of relief of the symptoms of multiple sclerosis by the use of
cannabis, we may see a rise in the number of cases of drug-induced
psychosis. There are no studies of treatment of the psychosis associated
with multiple sclerosis. Low doses of atypical antipsychotics such as
risperidone or clozapine should be the treatment of choice, as they have
fewer side-effects than the older antipsychotics. Clinical experience
suggests that benzodiazepines may also be used for sedation.
References:
McDonald WI, Compston A, Edan G, et al. Recommended
diagnostic criteria for multiple sclerosis: guidelines from the
International Panel on the diagnosis of multiple sclerosis. Ann Neurol 2001;50:121-7. doi:10.1002/ana.1032. PMID 11456302.
Meinl E, Krumbholz M, Derfuss T, Dewitt D.
Compartmentalization of inflammation in the CNS: A major mechanism
driving progressive multiple sclerosis. J Neurol Sci 2008;274: 42-4.
doi:10.1016/j.jns.2008.06.032. PMID 18715571.
This case in BMJ Case Reports shows both the level of superb
expertise of BMJ Case Reports and of the authors in presenting scientific
account of scientific methodology of diagnosis and treatment without story
building and ifs and buts. To the point addition to what had been known
earlier. It adds to our learning in the practice of medicine and gives a
feeling that there are journals with a difference and expert authors w...
This case in BMJ Case Reports shows both the level of superb
expertise of BMJ Case Reports and of the authors in presenting scientific
account of scientific methodology of diagnosis and treatment without story
building and ifs and buts. To the point addition to what had been known
earlier. It adds to our learning in the practice of medicine and gives a
feeling that there are journals with a difference and expert authors with
a difference who can do to the benefit of the patient conveniently and
teach with perfection.
This paper presents important information relating to treatment of Hydatid Cysts in liver and lung. Some of the hypotheses presented about diagnosis appeared doubtful.
1. In our case, iatrogenic cyst rupture triggered the development of an eosinophilic pleurisy.
The definition of eosinophillic pleurisy can be seen below;
Reactive eosinophilic pleuritis: a lesion to be distinguished from pulmonary eosinophilic granuloma....
This paper presents important information relating to treatment of Hydatid Cysts in liver and lung. Some of the hypotheses presented about diagnosis appeared doubtful.
1. In our case, iatrogenic cyst rupture triggered the development of an eosinophilic pleurisy.
The definition of eosinophillic pleurisy can be seen below;
Reactive eosinophilic pleuritis: a lesion to be distinguished from pulmonary eosinophilic granuloma.
Askin FB, McCann BG, Kuhn C. Arch Pathol Lab Med 1977;101:187-91
Abstract
Pleural nodules or sheets of histiocytes, admixed with eosinophils, giant cells, and other inflammatory cells are observed frequently in patients with spontaneous pneumothorax. This reaction, designated reactive eosinophillic pleuritis (REP), can closely resemble eosinophilic granuloma. Reactive eosinophilic pleuritis was found in pleural tissue of 22 of 57 patients with spontaneous pneumothorax in whom tissue was available for study. None of these patients had clinical or radiographic evidence of interstitial lung disease. Follow-up of 20 patients with REP ranged from six months to five years. None developed evidence of eosinophilic granuloma. Electron microscopy of one case did not show the Langerhans granules characteristic of the histiocytoses, including eosinophilic granuloma. Reactive eosinophilic pleuritit appears to be a nonspecific reaction to pleural injury, and is not a prodromal feature of pulmonary eosinophilic granuloma.
Authors did not present any biposy evidence yet claimed Eosinophilic Pleurisy.
2. Eosinophilia is found in less than 15% of patients and is generally only present following leakage of antigen from cysts. Without leakage too eosinophil count is rarely normal. One needs care count not eosiniphillia.
3. Figure 1, One view appears from surface plane and other through mid plane of cyst. To say non-cystic hydatid cyst is a neo-proposition perfectly indigestible.
4. A liver ultrasound scan detected a 35 mm lesion in the right lobe of the liver and at this point we proceeded to analyse hydatid serology. Was it an UltraSound for lung now and liver in next round and abdomen after some time and pelis after next time. Sophisticated instrument in hand, patient on table, procedure safe, facilities plenty becuse England: what could be harm to see all soft organs at one sitting particularly suspecting malignancy or paracytic cysts. How a liver cyst should be pathognomonic of hydatid while in lung it was diagnostic of malignancy on USG.
5. Complication could be avoided if Serology earlier or first.
How one can go to serology first if no suspicion of Hydatid. Should serology for hydatid be advisable for all the cases suspected carcinoma as in this case.
Hypotheses, hence, are lacking support for validity or reason.
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...
MRI in this case depicted tumor in a location where carcinoma is the most common neoplasm and lymphoma rare. Evidence is hardly of any use for readers unless microscopic evidence accompanied the MRI images. More important it was in view of the documentation that it was not typical lymphoid lesion in biopsy report but a lymphoepithelial mass; so, not necessarily neoplasm nor necessarily lymphoma, hence, awaiting final di...
Dear Editor,
I read with interest this article about intra-cranial dural venous sinus thrombosis, and many thanks go to the authors for the images.
Because the article is an "Images in...," I have the following notes:
The images do not tell which dural sinus (or sinuses) is thrombosed.
Pointing out to the abnormal areas on the images would be very helpful to the readership.
...Very significant cases of para neoplastic syndrome are described by authors, but, images of the tumors claimed to be the cause of the disease should have been shown for awareness of the reader experts of Medical Science for future utility to the benefit of the patients.
Conflict of Interest:
None declared
Here is a very good case of delayed contact dermatitis due to a known cosmetic allergen called Henna and hence this paper is also of public health significance. Allergen did take few days to precipitate allergic manifestations with dermatitis and eruptions which authors noticed to be infected and giving rise to scar formation which appeared like keloid due to oedema or hypertrophy. These changes, however, do not qualify...
Co-occurrence of psychosis and multiple sclerosis is uncommon. Most reports of psychoses and multiple sclerosis are single case studies. Literature review identified 39 case reports, a number that does not exceed chance expectation. This demonstrated that people with multiple sclerosis and psychosis are more likely to have plaques involving the temporal horns bilaterally.
Some studies suggested that psychosis in...
This case in BMJ Case Reports shows both the level of superb expertise of BMJ Case Reports and of the authors in presenting scientific account of scientific methodology of diagnosis and treatment without story building and ifs and buts. To the point addition to what had been known earlier. It adds to our learning in the practice of medicine and gives a feeling that there are journals with a difference and expert authors w...
1. In our case, iatrogenic cyst rupture triggered the development of an eosinophilic pleurisy. The definition of eosinophillic pleurisy can be seen below;
Reactive eosinophilic pleuritis: a lesion to be distinguished from pulmonary eosinophilic granuloma....
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