recovering after a week and after three weeks she was
able to sit, stand and walk.
Body righting reflexes are complex and these are five
separate types of reflexes (i) Labyrinthine righting
reflexes acting upon the neck muscle, (ii) Neck righting
reflexes acting upon the body (iii) Body righting reflexes
acting upon the head (iv) Body righting reflexes acting
upon the body (v) Optical righting reflexes. Center for (i)
to (iv) types of righting reflexes is in brain stem and for
optical righting reflexes is cortical.
Sensory impulses from proprioceptors of muscles,
tendons and joints are conveyed to the spinal cord by
medial division of the posterior roots and connects with
the cells of Clarke’s column and further continued
upwards in the dorsal (posterior) and ventral (anterior)
spinocerebellar tracts of the same side. Dorsal
spinocerebellar tract through inferior cerebellar
peduncle and ventral through superior cerebellar
peduncle reaches to the cerebellum. Impulses from
floculonodular lobe of cerebellum passes to reticular
formation in brain stem via fastigiobulbar tract (center
for body righting reflexes) and further through
reticulospinal tract to anterior horn cells message is
conveyed regarding regulation of tone of skeletal
musculature of extremities, trunk and neck to maintain
the posture of body (vegetative nervous system).2,3
Fig. 1 : MRI brain showing ring lesion.
Fig. 2 : Contrast MRI brain showing ring-enhancing lesion.
temperature, viberation, position and cortical sensations)
bilateral normal. Rhomberg sign positive (both open and
closed eyes), Cerebeller functions were normal. Position
of head in relation to trunk and body was normal and
she was able to lift the head.
On investigation: Urinalysis, Haemogram, Blood
biochemistry, X-ray Chest, E.K.G. were normal. M.R.I.
Brain (Plain and contrast) revealed a 6 X 5 X 5 mm. ringenhancing lesion with peri-lesional oedema (hypertense
on T2 weighted images) involving right side of caudal
brain stem in the paramedical area of dorsal medulla
sparing right restiform body (Figs. 1 and 2 ). Elisa for
cysticercosis was positive i.e. 0.55 OD (> 0.35 OD is
positive). Patient was treated with Albendazole 400 mg
twice a day for three weeks and Prednisolone 20 mg per
day for two weeks and thereafter tapered. Patient started
668
In this reported case, inflammatory lesion with perilesional oedema in the right side of caudal brain stem
with normal sense of position and vibration and
cerebellar functions i.e. sparing right restiform body may
have involved the center for body righting reflexes acting
upon the right side of the body. Peri-lesional oedema
must have subsided with prednisolone and relieved
pressure on the center in caudal part of right side of
brain stem, may explain the full recovery i.e. she was
able to sit, stand and walk properly. Available literature
was reviewed, such type of unilateral neurological
involvement i.e. unable to maintain upright posture with
normal motor and sensory system is not reported so far.
AK Gupta
Medical Specialist, Regional Hospital, Nahan, Himachal
Pradesh 173 001.
Received : 13.12.2005; Revised : 4.3.2006; Accepted : 7.7.2006
REFERENCES
1.
Magnus R. Studies on the physiology of posture. Lancet
1926;2:531-6.
2.
Magoun HW. The ascending reticular activating system. Res
Publ Ass Ner Ment Dis 1952;30:480-8.
3.
Best CH, Taylor NB. Spinal cord and brain stem. A Text
Book of Applied Physiology, 8 th ed (II nd Indian Reprint)
Calcutta, 1967;116-43.
Aortic Aneurysm : An Unusual Presentation
Sir,
Nowadays, superior vena cava syndrome (SVCS) is
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© JAPI • VOL. 54 • AUGUST 2006
believed to result almost entirely from malignancy, and
at presentation other causes of SVCS1 are overlooked or
underreported. Aneurysms and pseudoaneurysms of the
ascending aorta have been reported to cause SVCS.
Atherosclerosis is not commonly associated with
aneurysms of the ascending aorta2 even though it is the
usual cause of aneurysm of the descending aorta.3
Atherosclerosis as the cause of aneurysm of the entire
aorta is also unusual. We report a case of atherosclerotic
aneurysm involving the entire aorta presented with
SVCS, a rare clinical presentation.
A 52 years man with a history of heavy smoking was
admitted for evaluation of exertional breathlessness of 3
months duration. Physical examination revealed
features of obstruction of the superior vena cava (SVC)
and pleural effusion on the left side. His pulse rate, blood
pressure and temperature were normal. There were no
signs suggestive of any connective tissue disease. The
fasting lipids were: total cholesterol –282mg/dl, LDL
cholesterol –202mg/dl, HDL cholesterol –35mg/dl
VLDL –62mg/dl and the triglycerides –146mg/dl. Chest
radiograph revealed pleural effusion on the left side,
cardiac enlargement with a widened aortic shadow and
prominence of the superior vena cava (Fig. 1).
Electrocardiogram showed left ventricular hypertrophy
and transthoracic echocardiography showed dilated
aortic root, moderate aortic regurgitation and a left
ventricular ejection fraction of 70%. A computed
tomogram of the chest and abdomen showed fusiform
aneurysm involving the ascending, the arch and the
descending portions of the thoracic and the abdominal
aorta up to the common iliac arteries with multiple small
areas of calcification consistent with diffuse
atherosclerosis. Dilated ascending aorta was
compressing the superior vena cava causing the SVCS
(Fig. 2). There was no intra-thoracic or intra-abdominal
lymphadenitis and the lungs and the abdominal viscera
were normal. Other laboratory parameters (including
syphilitic serology) were normal.
The patient was advised aortic valve replacement and
aortic surgery with engraftment of the whole thoracic
aorta in a two-step procedure but he opted for medical
therapy. He was advised smoking cessation and
avoidance of strenuous activities and was prescribed
ramipril 5mg OD, aspirin 150mg OD, clopidogrel 75mg
OD and atorvastatin 20mg HS. After two months of
treatment, he reported some improvement in his
exertional dyspnoea and his lipid abnormalities showed
significant improvement.
Other than malignancy benign intrathoracic tumors,
inflammatory or infective processes, and a group of
cardiovascular diseases can cause SVCS. 1
Cardiovascular causes for SVCS are aneurysm of the
ascending aorta, dissection of the proximal aorta,
thrombosis of the SVC and rarely pseudoaneurysm of
the ascending aorta complicating aortic root surgery.
© JAPI • VOL. 54 • AUGUST 2006
Fig. 1 : Prominent SVC (arrow)
Fig. 2 : Arrow shows the compressed SVC
Ascending aortic aneurysms are seen in association with
familial disorders of collagen (Marphan syndrome,
Ehlers-Danlos syndrome and osteogenesis imperfecta),
syphilis, ankylosing spondylitis, mycotic aneurysms
caused by infections, trauma and coarctation of aorta.
This patient had extensive aneurysm involving
ascending and descending aorta and the etiology was
most likely atherosclerotic as supported by vascular risk
factors (cigarette smoking and dyslipidemia) and CT
scan findings. More so, there was no evidence of
connective tissue disorder and syphilis. Even though
SVCS and atherosclerotic aortic aneurysms are common
entities in clinical practice, atherosclerotic aneurysm of
the entire aorta presenting as SVCS is rare.
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669
Asha G Pillai*, J Thomas*, J Antony*,
MJ Pappachan**, G George***, P Sujathan+
diagnosis and treatment. Am J Crit Care 1992;1:54-64.
2.
Agmon Y, Khandheria BK, Meissner, et al. Is aortic dilatation
an atherosclerosis-related process? Clinical, laboratory, and
transesophageal echocardiographic correlates of thoracic
aortic dimensions in the population with implications for
thoracic aortic aneurysm formation. J Am Coll Cardiol
2003;42:1076-83.
3.
Reynolds HR, Tunick PA, Kort S, et al. Abdominal aortic
aneurysms and thoracic aortic atheromas. J Am Soc
Echocardiogr 2001;14:1127-31.
*Resident; **Senior lecturer; ***Associate professor;
+Professor, Department of Internal Medicine, Kottayam
Medical College. Kerala- 686 008.
Received : 16.3.2006; Revised : 5.6.2006; Accepted : 7.7.2006
REFERENCES
1.
Baker GL, Barnes HJ. Superior vena cava syndrome: etiology,
Announcement
36TH Annual Conference of Endocrine Society of India ESICON 2006, Jaipur 17th – 19th November, 2006
will be held at B.M. Birla Science and Technology Centre, Jaipur.
For further details please contact : Dr. R Patni (Chairman) or Dr. Prakash Keswani (Organising Secretary)
Secretariat : 399, Near Geeta Bhawan, Adarsh Nagar, Jaipur – 302 004.
E-mail : esicon2006@yahoo.com
Website : www.esicon2006.com;
Phone : 0141-2602342, 2612049
Announcement
XIIIth Annual Conference of API WB Branch at Hyatt Regency, Kolkata on 23rd and 24th September 2006.
Contact API WB Branch for registration
Prof. Samar Banerjee - Chairman, Dr. Surendra Daga - Hon. Secretary.
Tel: 033 2227 6024 / 6048
670
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© JAPI • VOL. 54 • AUGUST 2006