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Scorpion stings are a common problem in many parts of the world often reported from rural areas in developing countries like India. Here we report 2 cases from a particular locality of Western Orissa, received in different clinical states and studied the effect of Prazosin , which is its first trial report from this Medical College.

Clinical , experimental and laboratory investigations have confirmed the inter-relationship between stimulatory effects of the scorpion venom on Autonomic Nervous System (A.N.S) and adrenals and subsequent effect of released transmitters on C.V.S. The envenomation due to Mesobuthus tamulus , an Indian Red Scoripion sting can result in an acute life threatening medical emergency. It has been reported that the severity of Scorpion sting depends upon the time between the sting and administation of Prazosin. Prazosin , an alpha adrenergic blocker acts as a physiological antidote to venom of Scorpion.

Scorpion sting, Prazosin, Autonomic storm, Pulmonary edema.

Case No. 1
A 32 year male admitted to Medicine – III unit on 24/09/2005 being bitten by an Indian Red Scorpion over right occipital area, 5 cm from mastoid process while sleeping over a Log of wood at around 9 P.M. After ½ hour of the bite he had blurring of vision, dryness of mouth, burning sensation over lips, with 2-4 bouts of vomiting. He was confused at that time and unable to identify his relatives, with urinary urgency and retention of urine. Then he was transferred to a local hospital and treated with injection Hydrocortisone Deriphylline, Nikethamide, IV fluids and Oxygen. As the condition deteriorated he was referred to V.S.S. Medical College Hospital , Burla.
There was no history of fever, convulsion and patient was not a known case of Diabetes Mellitus, HTN, PTB, Sickle Cell Disease. He was a farmer by profession with no addiction to smoking or alcohol.
At the time of admission patient was conscious, afebrile. On examination Pulse – 148/min., regular BP 90 mmHg, systolic (diastolic not recordable), respiratory rate 40/min regular, abdominothoracic type. There was pallor, central cyanosis. There was no edema, lymphadenopathy, JVP was not raised, skin was cold and clammy with features of dehydration. Chest examination revealed B/L, normal vesicular breath sounds with basal crepitations . Heart sounds were normal without any murmur, P/A revealed abdomen soft, non tender and no organomegaly, CNS examination was within normal limit. Local examination at the site of bite revealed no abnormality.
Hb% -9.8gm%,DC-N 84%, L 16%, M0, B0, E0, ESR-08mm 1st hour, TLC-29,500/mm3 of blood
RBS-138mg%, Serum Urea-42mg%, Serum creatinine-1.9mg%
Serum Ca++-7.7mg%,-Serum Mg+-1.6mg%
Uric Acid -6.0mg%
Serum Bilirubin -T(1.6mg%), D (0.4mg%)
S.G.O.T-42 I.U./L, S.G.P.T.-52 I.U./L,S. Alkaline Phosphatase: 120 I.U./L
Chest X-Ray:
Showed shaggy heart borders with features of pulmonary edema. Echo study showed normal LV function with global hypokinesia, decreased LV systolic function, mild M.R., mild TR without PAH.
Within normal limit in all 12 leads.
Patient was treated with injection Dopamine , Dobutamin, Deriphyline, Ceftriaxone, Odansetron, Ranitin and O2 inhalation. Patient did not show signs of improvement till 2nd day of treatment. On 3rd day Prazosin (2.5 mg/day orally) started in low dose. Patient started improving, BP increased gradually, chest became clear. Then on 5th day Prazosin was increased to 5 mg/day orally and patient improved rapidly. On 7th day patient became completely asymptomatic. Repeat chest X-ray and Echo were normal and finally discharged with advice to continue Prazosin for another 7 days.
After 15 days patient attended OPD for follow up. He was totally asymptomatic , lungs were clear, blood pressure and CVS examination were normal. Finally Prazosin was stopped.
Case No. 2
A patient aged 40 years, a resident of village about 4 kilometers distant from 1st case was admitted on 29/09/2005 being bitten by an Indian Red Scorpion on right 2nd toe at around 9:30 P.M. He suddenly developed severe pain without local reaction at the site of bite. After half an hour he developed 2 episodes of vomiting and profuse sweating and severe breathlessness. He was taken to a local hospital and treated with injection Dopamine, Deriphylline, I/V fluids, Steroid. When he lost his consciousness he was referred to this Hospital.
At the time of admission patient was confused with pallor, central cyanosis, dyspnoeic, with respiration rate – 48/min abdominothoracic regular, Pulse – 110/min regular , BP – 100/60 mmHg , cold and clammy extremities. Systemic examination revealed B/L Vesicular BS, coarse crepitations on lung bases associated with rhonchi. Heart sounds were normal without any murmur, CNS examination revealed patient was confused without any cranial nerve and motor involvement. Plantar reflex was normal and DTR normal without any meningeal signs.
Hb% -8gm%, DC-N 87%, L 13%, E0, M0, B0, ESR-08mm 1st hour, TLC-25,400/mm3 of blood
RBS-156mg%, Serum Urea-22mg%, Serum creatinine-1.6mg%
Serum Na+-123meq/lit, Serum K+-3.8meq/lit
Ca++-7.8mg%, Mg+-1.9mg%
Uric Acid -6.2mg%
Serum Bilirubin -T(1.4mg%), D (0.3mg%)
S.G.O.T-44 I.U/L, S.G.P.T-58 I.U/L, S. Alkaline Phosphatase: 130I.U./L
Chest X-Ray: Within normal limit
ECG: Within normal limit in all 12 leads
Patient was treated with Tablet Prazosin 5mg injection Dopamin, Dobutamine, Deriphyline, Cefriaxone, Odansetron, Ranitin, O2 inhalation. Patient responded dramatically. On 3rd day he became asymptomatic with normal BP. Lungs became clear. Patient was stable on 5th day with normal vital signs and finally discharged on 4/10/2005.
Patient was followed up after one week. He was completely normal and Prazosin was stopped.
Indian Red Scorpion sting can present as an acute life threatening medical emergency often reported from rural areas. The sting frequently occurs at night because of Scorpion’s nocturnal habit.
Scorpion sting activates sodium neuronal channels causing excessive neuronal discharge.
The severity of Scorpion stings depends on patients age, season, the time between the sting and treatment with Prazosin. The signs and symptoms are due to potent autonomic storm in victims characterized by transient cholinergic effects1 – profuse sweating – hypersalivation, priapism in males, hypotension, bradycardia, ventricular ectopics and prolonged adrenergic effects – hypertension, tachycardia, cool extremities and pulmonary oedema. Vomiting , sweating, priapism and cool extremities are early diagnostic features of M. tamulus envenomation.
Pulmonary edema in Scorpion stings is of haemodynamic origin and related to a severe and prominent impairment of left ventricular systolic function.
Alpha receptor stimulation plays an important role in pathogenesis of Scorpion stings. Prazosin, an adrenergic alpha –1 blocker (invented in 1983-84) possesses pharmacologic properties that render it most suitable in antagonizing the toxic effect of Scorpion venom.
Prazosin reduces the pre-load and left ventricular impedance without rise in heart rate and rennin secretion3. It decreases pre-load and therefore causes no increase in cardiac output and heart rate contrast to hydralazine. It counters the action of local tissue liberated angiotensin – 2 in myocardium and also counters the vasoconstriction induced by liberated endothelin due to catecholamine excess by enhancing Nitric Oxide as a result of accumulation of C-GMP in vascular tissues by inhibiting phosphodiesterase. Scorpion venom inhibits insulin secretion which is counter acted by Prazosin.
Usual dosages2 is 250 mcg in children and 500 mcg in adults given to those having signs and symptoms of sever Scorpion sting irrespective of blood pressure provided there is no signs of hypovolemia.
From the above case report studies it was concluded that Prazosin reverses blood pressure, pulmonary edema irrespective of blood pressure and acts as a physiological antidote to scorpion venom.
1. Symptoms , Signs and Management of Indian Red Scorpion Envenomation – H.S. Bawasar , P.H Bawasar, Medicine Update , Vol No. 8, 1998, P 752 – 753.
2. Harrison’s Principle of Internal Medicine, Vol II, 16th Edition, P. 2604.
3. Bawasar H.S, Bawasar P.H., Prazosin in the management of Cardiovascular manifestation of scorpion sting – Lancet, 1986, P 510- 511.

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Organophosphorus induced delayed neuropathy (OPIDN) is a delayed sequel of organophosphorus poisoning, occurs rarely1,2,6 after an acute cholinergic crisis and is confused with Guillain Barre’ Syndrome (GBS) or other causes of polyneuropathy. We report one case of OPIDN which we managed conservatively with steroids & we found improvement of CMAP (Compound Muscle Action Potential) within one month.

Organophosphorus (OP), OPIDN, Axonal degeneration, neuropathic target esterase (NTE), Pralidoxim (PAM).

OPIDN refers to delayed effects of organophosphorus poisoning (OP poisoning), occurs due to binding of esterase enzyme called neuropathic target esterase (NTE)2,3 and cause predominant axonal degeneration (dying back axonopathy5) and minor demylenation7. Typically patient presents 3-5 weeks after OP poisoning with lower extremity weakness, bilateral foot drop, glove and stocking type of sensory loss5. Present case study documents one case of OPIDN due to tri Ortho cresyl phosphate poisoning after one month of cholinergic crisis and prevention of OPIDN is by early treatment of cholinergic crisis with PAM (before organophosphorus compound ages), steroids and other supportive measures (e.g splintage, physiotherapy and carbamazepine for neuropathic pain).

A 19 year male presented to the hospital with complains of tingling sensation and weakness of lower limbs and hands 15 days back. He was apparently alright 15 days back, had 4 episodes of loose motion which subsided with medication. Then he had tingling sensation over lower limbs and hands and weakness of lower limbs followed by weakness and clumsiness of both hands. Weakness was progressive and in one week the patient was not able to walk. No history of fever, dog bite, vaccination, previous similar episode, contact, diabetes, leprosy was elicited.

Allegedly he took insecticides and suffered from acute cholincrgic crisis one and half month ago for which he was hospitalized for 11 days and recovered. On general examination the patient was conscious, afebrile with pulse rate 80/min, BP 126/80mm Hg without any other positive findings. CNS examination revealed intact cranial nerves, wasting of hypothenar, thenar (Fig. 1), calf and peroneal muscles of limbs (Fig. 2). Hypotonia involving flexor and extensor of ankle, weakness of abductor pollicis berevis, adductor pollicis and oppones pollicis seen. Long flexors and extensors of digits were normal. Lower limbs evertor, invertor, flexor and extensor of ankle were 0/5 power on both sides. Extensor and flexor of knee and hip were normal. Supinator jerk was diminished, ankle jerk was absent on both sides. Rest deep tendon jerks were normal. Plantar was nonresponsive both sides. There was in-coordinated movement, Rhomberg's test was positive and gait was high stepping. Sensory examination revealed all modalities diminished below ankle and wrist bilaterally. Peripheral nerves were normal.

Laboratory investigation revealed:
o Hb 12.7 gm%, TLC 10,700/mm3, DC N-69 L-30 E-l, ESR 8mm/lst hr, FBS 85 mg% .
o Serum Na'-132meq/lt, Serum K-4.8meq/lt, Serum urea -28mg%, Serum creatinine -1.18 mg%.
o HIV ELISA - Negative, CSF study showed TLC 3/mm3 (all lymphocytes) RBC absent, Glucose 61mg%, Protein 27 mg%, TB ELlSA- Negative.

Initial Nerve Conduction Study:
Motor - Compound muscle action potential (CMAP) was absent in bilateral Median, Common peroneal nerve (CPN) , bilateral posterior tibial nerve (PTN).
CMAP in bilateral ULNAR - Amplitude less than normal, velocity in right ulnar less than normal , Left ulnar velocity within the normal limits.
Sensory - In bilateral Median Velocity was reduced, Right ulnar velocity was reduced no potential in Right sural, left Sural velocity and amplitude within normal limit.

Repeat Nerve conduction Study: (After one month)
CMAP- left median no potential, Right median small amplitude potential
Velocity in the above is reduced
Conduction in bilateral ulnar as before
No CMAP in bilateral CPN and bilateral PTN
Sensory as before

Chronic complication of OP poisoning are neurobehavioral and poly-neuropathy1. Sensory motor polyneuropathy or OPIDN typically ocours after 3 to 5 weeks of exposure where motor deficit dominates the clinical picture5. Patient initially complains of tingling sensation over extremities, symmetric lower extremity weakness, and leg cramping and calf pain. Atrophy of calf muscles, ataxia and bilateral foot drop gradually ensues. It may progress to cause truncal weakness. Cranial nerves and autonomic system are not involved3. Sensory symptoms resolve over months. In mild cases motor symptoms may resolve over 15 months or may not resolve at all3. Severe cases may develop spasticity due to spinal cord involvement in the form of diffused spinal cord atrophy predominantly of thoracic spine2,5. Neuropathology of OPIDN demonstrates that large distal neurons tend to be affected first. There is slowing and stoppage of axonal flow, blockage transport of protein and other substances as well as demyelination7. Axonal degeneration precedes demyelination and there is "dying back" axonopathy5. Site of OP attack is a membrane bound target esterase called neuropathic target esterase (NTE)2,3. Function of NTE is not known. It is present in brain, spinal cord and peripheral nerve6, lymphocytes4 where specific OP binds and ages1 by losing 1 carbon and forming P-O carbon linkage. Critical mass of 70% of NTE must be inhibited to cause clinical symptom6. The delay in symptoms is due to the fact that not all axons will degenerate at the same time and nerve may continue to function until significant number of axons is degenerated.

OPIDN diagnosis is made by clinical and neurophysiologic examination and ruling out other possibilities. Currently platelet, RBC and lymphocyte NTE inhibition for confirming neuropathic potential of organophosphorus is under study . Use of hen test as screening test of neurotoxicity is flawed1.

Treatment of OPIDN is conservative and can be prevented by early and prolonged use of PAM. Tingling sensation over palm and sole responds to carbamazepine5.

1. Angelo Moretto et al: Poisoning by organophosphorus insecticides and sensory neuropathy; J. Neurol. Neurosurg. Psychiatry: 1998;64;463-468.
2. Cnia-Chang Chuang et al: Delayed Neuropathy and Myelopathy after Organophosphate Intoxication: NEJM, Volume 347:1119-1121 October 3, 2002 Number 14.
3. J. Mirandal et al : Muscular Strength and vibration thresholds during two years after acute poisoning with organophosphate insecticides. Occupational and Environmental Medicine BMJ 2004; 61: e4.
4. M. Lotti et al: Inhibition of lymphocyte neuropathy target esterase predicts the development organophosphate induced delayed polyneuropathy:J. Arch of Toxicology, Vol 59/3 Oct 1986, Pg 176-179.
5. R. Hierons and M.K. Johnson : Clinical and Toxicological investigations of a case of delayed neuropathy in man after acute poisoning by an organophosphorus pesticide: J Arch of Toxicology, Issue Volume 40, Number 4/Deceber , 1978.
6. Singh H, Sharma N: Neurological Syndromes Following organo-phosphate poisoning, Year 2000 , Neurology India, Volume 48, issue 4, Page 308-13.
7. Versik P et al: Chronic Toxic Neurophaty in Qualis: British Lek Letsy 106 (10), 293 – 296, 2005.

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Acute Inflammatory Demyelinating Polyneuropathy following Malaria is a rare clinical presentation. Few cases have been reported so far from India and abroad. Here we report such a case from this hospital and discuss the pathophysiology and management.

Acute inflammatory demyelinating polyneuropathy (AIDP),
Plasmodium falciparum,
IV immunoglobulin.

Acute inflammatory demyelinating polyneuropathy (AIDP) is acute, frequently severe and fulminant which is auto immune in nature characterized by rapidly developing areflexic ascending motor paralysis with or without sensory disturbances. 75% of cases are preceded 1-3 weeks by an acute infectious process usually respiratory or gastrointestinal. The reported microorganisms include Campylobacter jejuni, Mycoplasma, Human herpesvirus, CMV, E-B virus etc3. The AIDP following malaria is of rare occurrence. However recently several cases have been reported following both vivax and falciparum malaria1,5.

A 16 years boy from sonepur was admitted to this hospital on 18.06.2006 with complains of sudden weakness of both lower limbs and both upper limbs and inability to walk for 10 days. Twelve days back he had fever with chill and rigor for which he consulted local physicians and detected to be a case of Falciparum Malaria (slide +ve) and treated with chloroquine tablets. Next morning the patient noticed weakness and tingling sensation of both lower limbs. He was treated with IV fluids and multivitamin injection. The weakness rapidly progressed and after 2 days he developed weakness of both upper limbs and paralysis of both lower limbs leading to inability to walk. He was treated at the District Hospital with antimalarial drugs and referred to this Hospital.

On admission the patient was febrile (Temp. 99.80 F) conscious. There was mild pallor without icterus, clubbing, cyanosis, oedema or Thyroid enlargement. Pulse was 96/min, regular, B.P. was 120/80mm of Hg in both upper limbs. Respiration rate was 16/min. and abdominothoracic type. There was no sign of dehydration.

Neurological examination revealed normal higher intellectual functions with all cranial nerves intact without any pupillary abnormality. Motor examination showed normal bulk and tone of all muscles in upper and lower limbs. Power in both upper limbs were 3/5 grade in proximal groups and 4/5 grade in distal groups including hand grip weakness. Power in both lower limbs were 2/5 grade in proximal group (flexor, extensor around hip) and grade 3/5 around knee, ankle and feet. Power in trunk muscle and abdominal muscles were normal. Bladder and bowel were not involved. Coordination could not be tested and there was no involuntary movement. Deep Tendon reflexes in all four limbs were absent. Plantar was non responsive in both limbs. All the superficial reflexes were absent. Gait and Romberg’s test could not be done due to weakness. Sensory system examination showed all modalities intact. Autonomic nervous system was normal. Skull and spine was normal without any sign of meningitis.

Respiratory system, cardiovascular system, gastrointestinal system and other systems were normal.

There was no such past history. There was no history of SCD, TB, DM, HTN, exanthematous fever or dog bite. Family history was not suggestive.

Routine examination findings were-
HB – 9gm% ,TLC – 10,200/mm3, DC – N-64, L-30, E-6, M-0, B-0, ESR – 46mm 1st hour
ICT for Malaria – PFR ++
Serum – Na+ - 138m Eq/l, K+ - 4.2m Eq/l, Ca+ - 8mg%
Serum urea – 46mg%
Creatinine 1.5mg%

LFT – Serum Bilirubin – 1.3mg%(Total), 0.4mg% (Direct), SGOT- 42 IU/L, SGPT-97IU/L, Alkaline Phosphatase - 548IU/L. Chest X-ray PA view and X-ray of Lumbosacral spine were normal . Ultrasonogram of abdomen and pelvis was normal. CSF was clear with normal pressure, CSF cell count was 12/ml mostly lymphocytes, Glucose was 58mg%, protein 240mg% and gram stain and AFB were negative. Nerve conduction studies in both median, ulnar and common peroneal nerves revealed gross reduction in amplitude and motor nerve conduction velocity. The distal latency was grossly prolonged in all the nerves. F waves were absent in all the nerves. The sensory conduction in both median and common peroneal nerves was absent.

The patient was diagnosed to be a case of AIDP fllowing falciparum malaria. He was treated with full course of injection Artesunate and IV immunoglobulin 20g/day for 5 days. The patient improved after 3 days of completion of immunoglobulin . The power in all four limbs improved. On 10th day of admission the patient was discharged with follow up advise.

Acute inflammatory demyelinating polyneuropathy (AIDP) are seen following viral, bacterial infections or immunization and is uncommon following parasitic infection like malaria2. It is important to rule out other neurological syndromes that may be unmasked by febrile episode.

The pathogenesis of AIDP following malaria is not known. This is likely to be immunogenic that occurs after viral/bacterial infections.

Other possible mechanisms suggesting development of polyneuropathy following a parasitic infestation include:
• Parasitic emboli obstructing vasa nervosum.
• Release of neurotoxins.
• Associated metabolic and nutritional disturbances.
• Immune mediated capillary damage.
• Release of free radicals and tumors necrosis factor.

AIDP is a variant of GBS manifests as rapidly developing areflexic motor paralysis with or without sensory disturbances. The pattern is ascending type and first noticed as rubbery legs. Weakness typically evolves over hours to few days and frequently associated with tingling dysesthesia in extremities.

Legs are affected more than arms. All the reflexes are absent. Lower cranial nerves are frequently involved. Bladder involvement is rare. In severe cases autonomic dysfunction may occur, resulting in fluctuation of blood pressure, postural hypotension, cardiac dysrythmias.

Modified A.K. Asbury Criteria (for GBS):
Required Criteria:
• Progressive weakness of 2 or more limbs due to neuropathy
• Areflexia
• Disease course < 4 weeks
• Exclusion of other causes like vasculitis, botulism, diphtheria, porphyria, cauda equina syndrome.
Supportive Criteria:
• Relatively symmetric weakness
• Mild sensory involvement
• Facial or other cranial nerve involvement
• Absence of fever
• Typical CSF profile (Acellular , Increase protein level)
• Electrophysiological evidence of demyelination

Treatment is to be given as early as possible. In > 2 weeks of first motor symptoms, immunoglobulin is not effective. IVIg is administered as five daily injections for a total dose of 2g/kg body weight.

A course of plasmapheresis consisting of 40 to 50ml/kg, plasma exchange four times a week is usually employed. Combination has no advantage. Steroid has no role. In worsening phase critical care and ventilatory support is required.


In conclusion we report that falciparum malaria may present as AIDP and this possibility though uncommon must be taken into consideration while encountering patients in endemic areas.

1. Kanjalkar M, Karnad DR, Namayan RV, Shah PU: Guillain-Barre Syndrome following malaria, J. Infect 1999; 38: 48-50.
2. Sokrab RT, Eltahir A, Idris MN, Hamid M: GBS following acute falciaprum malaria, Neurology 2002, OCT, 22; 59(8), 1281-3.
3. Harrison’s Principle of Internal Medicine, 16th Edition, Vol – II, ; 365: P2513-14.
4. Corner DH, Herber JM, Parasitic infections of the pripheral nervous system in: Dyck PJ, Thomas PK, eds. Peripheral neuropathy, Philadelphia: WB Saunders; 1993 PP. 1338 – 90.
Chakravarty A, Ghosh B, Bhattacharyya R, Sengupta S, Mukherjee S: AIDS following

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Delayed cerebellar ataxia is a rare acute self limiting complication of falciparum malaria [2]. This complication is predominantly found in Sri Lanka though few cases have been reported from India and Africa [2,4]. We have recently encountered such a patient in our hospital. The case is described below with pertinent literatures reviewed.

Delayed cerebellar ataxia, Plasmodium falciparum

Delayed cerebellar ataxia found in falciparum malaria is usually an acute self limiting and isolated ataxia without cerebral involvement [4]. The patient usually shows features of midline cerebellar involvement and is characterized by cerebellar gait and truncal ataxia [1,4]. Most of the patients are afebrile before the onset of symptoms [1,4].

A 45 year old engineer was admitted to the hospital in September '07 with complaints of difficulty in maintaining balance with a tendency to fall in all directions for the past four days. He developed high grade fever, intermittent in nature associated with chills and rigor and subsided with profuse sweating. He was admitted in the local hospital and was detected having falciparum malaria by MP slide and was treated with anti-malarials and antibiotics. The patient became afebrile after five days and was discharged. Four days later He developed instability of gait such that he lurched and fell in all directions – this left him unable to walk. He was then referred to our hospital for further investigations and management.
There was no history of diabetes mellitus, hypertension, tuberculosis or sickle cell disease.

Family history is also not suggestive of diabetes mellitus, hypertension, tuberculosis or sickle cell disease.

On admission the patient was found to be conscious afebrile. There was mild pallor, no cyanosis, icterus, clubbing, edema, Lymph node or thyroid enlargement, JVP was not raised, Pulse was 80/ min regular, B.P. 150/ 84 mm of Hg, Respiratory rate of 18/ min and temperature was 36.4 ° C.

Neurological examination revealed normal higher mental function. All cranial nerves were found normal. Motor system examination revealed normal bulk, tone and power. The gait was broad based with irregular stepping and a tendency to fall in all direction. No sensory impairment or autonomic involvement was found. On finger nose testing revealed past pointing; the knee heel shin test was found to be clumsy bilaterally. Disdiadochokinesia was present bilaterally. The deep tendon reflexes were normal, plantar was bilaterally flexor. The cranium and spine was normal and there were no signs of meningeal irritation.

The respiratory, cardiovascular, and gastrointestinal system was found to be normal.

On investigation Hb% was 11.2 gm/dl, DC N72 E3 L25; Total leukocyte count was 7100/cmm and ESR was 6 mm in 1st hr. Routine blood biochemistry  Fasting blood glucose 110 mg/dl, urea 28 mg/dl, creatinine 1.4 mg/dl, serum Na+ 147mEq/l and K+ 4.0 mEq/l. Malaria parasite by ICT was found to be positive. CT scan of brain was found to be normal and no abnormality was detected by pure tone audiometry bilaterally. CSF study was found to be normal.
The patient was diagnosed as having delayed cerebellar ataxia following falciparum malaria. He was treated with a full course of inj. Artesunate for 5 days. The patient rapidly improved and by the 5th day he was able to walk on his own. The cerebellar signs disappeared on the 6th day and he was discharged with advice after 7 days of admission.

Neurologic features found in malaria are usually not consistent; the commonest being altered sensorium followed by seizures [1]. But cerebellar involvement is the most consistent neurological manifestation of complicated as well as uncomplicated malaria as Purkinje cells are susceptible to damage due to hyperpyrexia [4].

RBCs with parasitized P. falciparum adhere to the endothelial wall of capillaries in a certain phase of its cycle. Parasites derive some nutrition from endothelium. This phenomenon occurs maximally in the capillaries of brain [1]. Focal hemorrhage or non hemorrhagic infarcts in cortex, basal ganglia, thalamus, pons and cerebellum have all been described in cerebral malaria [1]. Immunologic mechanism, as a cause for delayed cerebellar ataxia has been postulated; cerebellar demyelination following falciparum malaria has been reported in several patients from Sri Lanka and India occurring several days after recovery [1,4]. The CT scan of brain is normal [1,2]. The disease has an excellent prognosis with complete recovery in 3 months [2,4]. The patients are treated symptomatically though some physicians prefer to use steroids.

Cerebellar involvement in falciparum malaria may be due to selective clogging of cerebellar micro vasculatures with parasitized RBCs, perivascular hemorrhage, microscopic infarcts, shrinkage of purkinje cells and perivascular clusters of microglia, carrying a high mortality rate [1,3] or, may be due to immunologic mechanism as in the case of delayed cerebellar ataxia [1,4].

Delayed cerebellar ataxia is a rare complication of cerebellar involvement following falciparum malaria and may be considered in the differential diagnosis in patients showing cerebellar signs especially if the patient gives a past history of fever. This is the first reported case of delayed cerebellar ataxia from our institution.

1. Adult cerebral malaria: prognostic importance of Imaging findings and correlation with postmortem findings; Tufail F. Patankar, MD, Dilip R. Karnad, MD, Prashant G. Shetty, MD, Anand P. Desai, MD, Srinivasa R. Prasad, MD;Radiology 2002;224:811-816
2. Delayed cerebellar ataxia following Falciparum malaria: Hussam Alsoub, MD : Annals of Saudi Medicine,1999;Vol 19, no. 2: 128-129
3. MR of cerebral malaria; Yves Sébastien Cordoliani, Jean-Luc Sarrazin, Dominique Felten, Eric Caumes, Cristophe Lévêque, Alain Fisch; AJNR Am Neuroradiol 19:871-874, May 1998

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Neurocysticercosis is most common parasitic infestation of CNS1. The incidence of spinal involvement is 1.5-3%4.Spinal neurocysticercosis usually appear due to mass effect. Most cases occur in subarachnoid space but intra medullary location is extremely rare1. Here we report a case of intramedullary neurocysticercosis (reported about 50 cases sofar) 4 and discuss the disease.


Neurocysticercosis (NCC), Spinal neurocysticercosis (SNCC), intra medullary, Tinea Solium, MRI.

A 26 year named BC , from Salepur presented to this hospital in June 2008 with c/o of head ache & neck pain(1 month), numbness of right side of face(15 days),inability to hold objects properly in right hand (15days).He was alright 1 month back. Started with continuous headache relieved with analgesics, without associated vomiting, nasal stuffiness or blurring of vision. After 15 days he developed numbness of right side of face & noticed weakness of right hand which gradually progressed so that he could not hold any object properly. There was no history of fever, root pain, or convulsion. There was no bladder or bowel involvement. There was no h/o Diabetes, trauma, hypertension or tuberculosis. Family history was not suggestive. He was not habituated to alcohol or smoking. There was no contact history& he was unmarried.
On examination he was of average built having BP- 130/80 mm of Hg; pulse 68/ min, regular; without pallor, jaundice or lymphadenopathy.
CNS examination revealed patient to be conscious with normal higher functions including speech. All the cranial nerves were intact except diminished pain sensation on right side of face. Motor system showed normal bulk with increased tone of muscles in legs & arms. Power was grade V in both lower limbs but grade IV in both upper limbs. Hand grip was weak on both sides, right >left. Bicep & triceps reflexes were exaggerated on both sides with normal supinators. Knee & ankle jerks on both sides were exaggerated. Plantar was extensor on right but flexor on left. Sensory system was normal. Skull & spine was normal without any meningeal or cerebellar signs. Fundus was normal.
Other systems like CVS, GIT, respiratory did not reveal any abnormalities.
Routine investigations like Hb%, DC, TLC, FBS, urea, creatinine serum K+, Na+ were normal. ESR was 25/1st hour & Mx was negative. Chest X-ray & cervical spine X’ray were normal. CSF study was normal. MRI of brain & spinal cord showed ring enhancing tiny lesions at cervico medullary junction inside the medullary central canal with consequent syrinx formation..(Figure-1,Figure-2) Anticystocercal antibody was positive.
A young male presenting with gradual onset of assymetrical weakness of upper & lower limbs, with headache & diminished pain sensation of right side of face without significant involvement of lower limbs with features of UMN involvement in the form of hypertonia & hyper reflexia of all limbs below C4 without sensory level a provisional diagnosis of high cervical cord compression ( intramedullary) was thought of, probably involving trigeminothalamic tract(right) & corticospinal tract below pyramid (right). With the investigations the patient was diagnosed as a case of SNCC with obstructive syringomyelia.
The patient was treated with Albendazole 400 mg twice daily for 28 days with oral prednisolone in tapering dose.In the next followup after one month he complained of progressive weakness of upper limbs with no response to Albendazole.Hence he was advised for neurosurgical consultation for excision of the cyst.
Neurocysticerosis is the most common parasitic infestation of CNS caused by ingestion of eggs of Taenia Solium3.T.Solium has its definite host in human being where adult worm stays in intestine laying eggs which are taken by pigs who are intermediate hosts. The embryo cross the intestine and reside in CNS, muscles, eyes and skin as cysticerci.Human beings have the disease when they ingest the eggs instead of Pigs. The eggs hatch in the intestine and develop into cysticerci in the above mentioned organs.

Usual organs involved in Neurocysticerosis are brain, eye, subcutaneous tissues.Common presentation of cysticerosis of brain are headache, seizure and focal neurological deficit.

Spinal neurocysticerosis is a rare presentation; the incidence ranging from 0.7-5.85%1,3.Spinal forms have been identified in vertebral, extradural, intradural, intramedullary regions.Intramedullary cysticerosis is very uncommon1. Migration of the cysticercus through the ventriculo-ependyal pathway and haematogeneous dissemination has been identified as pathogenic mechanism1,4.

In absence of previous history or subcutaneous nodule it may be difficult to suspect clinically intramedullary cysticerosis.High eosinophil count with soft tissue calcification though suggestive is rare.Result of surgery has not been encouraging due to parenchymal gliosis as a result of toxic waste from larva, pachymeningitis and vascular insufficiency.
But in the era of microsurgery good outcome has been reported. Medical treatment of intramedullary lesions can be considered in patients of stable neurological status but impossible in acute or progressive cases.Post operative anticerceal drugs should be given as it is a generalized disease with focal manifestation1.
SNCC is rare compared to intracranial as cysticerci do not pass through subarachnoid space at cervical level due to its size(sieve effect).Besides CSF reflux at craniovertebral junction propels floating cysts back into intracranial space than spinal canal.

Several possible mechanisms of spinal invasion are:-
(a)Ventricular cysticerci pass through Magendie or Luschka foramen, migrate by gravity through subarachnoid space to inoculate spinal cord commonly cervical region.
(b)Haematogeneous spread explain intramedullary lesion,commonly thoracic area due to increased blood flow.(c) Intraventricular hypertension enables migration through a dilated ependymal canal into spinal cord explaining intramedullary invasion.Other favorable conditions favoring spinal invasion may be due to NCC-related hydrocephalus and/or meningitis, use of antiepileptic drugs like Carbamazepine or Phenytoin which can after immune function leading to parasitic infestation3.

The location of mass lesion, its size, the inflammatory response generated by cyst breakdown are important factors for management.Brain blood flow is 100fold greater than spinal explaining more intraventricular lesion.In spinal form thoracic region having more blood flow explains high incidence.The location of cysticerci is cervical - 34%,thoracic -44.5%, lumbar -15.5% and sacral- 6%.MRI is the investigation of choice.
Concurrent intracranial lesion are seen in spinal involvement. As long as cysticercus is viable there is relative host immune tolerance. Massive antigen response occurs with death of parasite with intensification of immune/inflammatory response.Surgery is required for diagnosis and treatment though outcome is mixed. Albendazole or Praziquantel with or without steroid are used. Albendazole is preferred as blood level are increased with steroid.Spinal intramedullary cysticercosis represents a challenge for diagnosis & surgery. Patient recovery is variable. Despite promising reports the safety and efficacy of medical treatment remains unproved4.

1. Singh P, Sahai K.-Intramedullary cysticercosis.Neurol India 2004;52:264-5
2. Mohanty A.Venkatrama SK, Das BS,Rao BR,Vasudev MK -Spinal Intramedullary cysticercosis-Neurosurgery.1997; Jan 40(1):82-7
3.Dong Ah Shin & Hyun Chul Shin-Yonsei Med.J.2009,Aug 31;50(4):582-584.
A case of extensive spinal cysticercosis involving whole spinal canal with a h/o cerebral cysticercosis.
4.Agarwal R,Chauhan SPS, Mishra V, Singh PA,Gopal NN-Acta biomed 2008;79,39-41
Focal spinal intramedullary cysticercosis.

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Primary 1. Association of serum Ca++, Mg++ level in cases of hypokalemic disorder.
Secondary 2. Response of treatment with potassium supplementation and Mg++ and Ca++ requirement.

Fifty cases of hypokalemia, most of them having history of hypokalemic periodic palsy, were taken for study, in department of medicine for November 2003 to April 2005. Detail clinical history, physical examinations and routine laboratory investigations done including mandatory serum Na+, K+, Ca++, Mg++. The laboratory investigation of serum electrolytes were repeated after 2-3 days of K+ supplementation and in resistant hypokalemic cases with magnesium deficiency, Mg++ supplementation was given first and then Ca++ supplementation in combined Ca++ deficiency cases.

Out of the 50 patients, 25% were males (30-60 years), 40% were females 18-40 years. Commonest presentation were paraplegia (75%), Quadriplegia (25%), vomiting (20%), Hicough (4%), Tetany (2%), Bradycardia (6%), Paralytic ileus (2%) and various ECG changes ie. U wave, increased PR interval, decreased T wave etc. Most of the patients belonged to low socio-economic status and most of them were physical labourers. In moderate to severe hypokalemia, hypomagnesemia was commonly present ( 64%) and hypocalcaemia (28%). Most of these cases responded to K+ supplementation but in some cases with severe hypokalemia associated with hypomagnesemia and hypocalcaemia were resistant to K+ supplementation. In these cases long with K+ , Mg+ supplementation was given, after which patients responded rapidly and satisfactorily. Dramatic improvement was seen in the power of limbs after supplementation of K+. However n 6% patients no significant improvement was seen after 2-3 days and Mg+ was supplemented orally after which there was improvement in power of limbs and serum K+ level rapidly.
Hypokalemia Hypomagnesemia Hypocalcemia
Mild (3.0-3.5 meq/l) 3(6%) 0(0%)
Moderate (2.5 – 3.0 meq/l) 7(14%) 6(12%)
Severe(<2.5 meq/l) 22(44%) 8(16%)

(Incidence of Hypomagnesemia and hypocalcemia according to severity of hypokalemia)

It was observed that in hypokalemic disorders there is derangement of other electrolytes (i.e Serum , Mg++, Ca++). In moderate to severe hypokalemia estimation of serum Mg++ and Ca++ is mandatory and Mg++ replacement should be done after K+ supplementation and before Ca++ supplementation in combined electrolyte disorders to avoid arrythmia.

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Lp (a) a cholesterol ester rich LDL like particle that contains apo B 100 linked by disulphide bridge to a highly polymorphic glycoprotein  apolipoprotein. Lp(a) has both atherogenic and thrombogenic properties. In this study serum Lp(a) of Coroanry artery disease patients were correlated with of controls to find out any correlation between Lp(a) and Coronary Artery Disease.


In the present study 50 percent of cases of newly detected Coronary artery disease with various presentations of acute coronary syndrome (ACS) like unstable angina, NSTEMI & STEMI were taken. Cases were confirmed by clinical criteria, ECG and increased cardiac markers. Lp(a) level was estimated by Nephelometric method. Sample taken either within 6 hours of onset of symptoms or after 28 days of onset of symptoms. 30 suitably age and sex matched controls were taken having no evidence of coronary artery disease and their Lp(a) level estimated. Serum lipid profile (TG, Cholesterol, VLDL, LDL, HDL) were also estimated.


The mean age of the patients in the study was 55.4 years (45-70 years). Anteroseptal MI was predominate (42%) followed by inferior wall MI (28%), anterolateral MI (26%), inferior & RV MI in 4%. Distribution of different risk factors were smoking in 52%, DM in 12%, hypertension in 24%, family history of CAD in 13%, hypercholesterolemia in 24% and hypertriglyceridemia in 17%. In the present study the mean serum Lp(a) in cases was (28.86.0 mg/dl) and the control group was (18.34.0mg/dl) with P value < 0.01).


Patients of coronary artery disease group had significantly higher level of Lp(a) in comparison to controls without coronary artery disease establishing the role of serum Lp(a) as an independent risk factor for coronary artery disease.

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AIDP following Malaria is a rare clinical presentation. Few cases have been reported so far from India and abroad. It is usually acute onset with rapidly developing areflexic ascending motor paralysis with or without sensory disturbances. Though various mechanisms are postulated it is more likely immunogenic. It responds to I/V immunoglobulin along with anti malarial therapy. Early therapeutic measures lead to good prognosis.

A 16years boy admitted on 18.06.2006 with sudden weakness of all four limbs following 2 days of fever with chill and rigor. Detected to be Falciparum malaria (slide test) and treated locally with chloroquin referred to this hospital.

On admission the patient was febrile, conscious with mild pallor. Other vital signs were normal. Respiratory, CVS and Gastrointestinal system were normal. Neurological examination revealed normal higher intellectual functions without any cranial nerve involvement or pupillary abnormality. Motor examination showed normal bulk and tone of all muscles. Power in both U/L were 3/5 in proximal and 4/5 in distal groups including handgrip weakness. Power in both lower limbs were 2/5 around hip and 3/5 around knee, ankle and feet. There was no abnormal movement. Deep tendon reflexes were absent in all four limbs. Plantar was nonresponsive. All superficial reflexes were absent. Sensory system, autonomic nervous systems were normal without bladder and bowel involvement.

Routine blood examination findings showed Hb- 9gm%, ICT for malaria- PFR ++ and DC, TLC, ESR were normal. Serum electrolytes, urea, creatinine, FBS, and LFT were normal. Chest X-Ray, X-Ray of L.S. Spine and USG of abdomen and pelvis were normal. CSF picture was normal. Nerve conduction study of both median, ulnar and common peroneal nerves revealed gross reduction in amplitude and motor nerve conduction velocity, with prolonged distal latency, and absence of F waves. Sensory was absent in all the nerves.

The patient was treated with full course of injection Artesunate and IV immunoglobulin 24g/day for 5 days. The patient improved after 3 days of completion of immunoglobulin. The patient was discharged in 10th day of admission after fully recovery.

AIDP is seen following viral (herpes virus, CMV, E-B virus etc) bacterial (Campilobacter jejuni, Mycoplasma) or immunization. But it is uncommon following parasitic infection like malaria. It is important to rule out other neurological syndromes that may be unmasked by febrile illness. The pathogenesis of AIDP following malaria is not known. This is possibly to be immunogenic like that occur after viral or bacterial infection. Other possible mechanisms of polyneuropathy may be due to parasitic emboli obstructing vasa nervosum, release of neurotoxins, associated metabolic and nutritional disturbances, immune mediated capillary damage, and release of free radicals and tumor necrosis factors.

AIDP is a variant of GBS encountered rarely following malaria (few case reports after Vivax, Falciparum). Early institution of I/V immunoglobulin results full recovery. Steroid has no role.

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Cardiac involvement is a well established fact in extensive pulmonary tuberculosis. However, there are few references available in this regard to throw light on the early stages of tuberculosis.

Keeping this in mind the present study was undertaken in the Dept. of Medicine and TB & Resp. Diseases of V.S.S. Medical College, Burla to observe.

1. The Electrocardiographic changes at the time of diagnosis of pulmonary tuberculosis.
2. The effect of ATT on ECG changes.
3. The possible cause of reversibility.


Selection of patients included all sputum positive pulmonary tuberculosis during 3 years period. Patients having pre-existing cardiac disease, under cardiac glycosides, severe anaemia, pregnancy were excluded from the present study. Patients having other respiratory disorder or any pleural complications were also not included.


90 cases were taken up in the present study out of which sinus tachycardia (66.6*), sinus bradycardia (4.44%), low voltage & afcjnomial axis (13.3%), S.T. segment depression (11.11%). RVH (8.88%), T. inversion (8.8b%), SSS Syndrome (6.6%) cases were observed.
The exact mechanism of ECG changes is unknown. However the possible explanation could be fever, toxaemia, Broody's effect, direct myocardial involvement, tymphadenopathy causing irritation of uonomic nerve fibres in the hilum and consequent altered sympathetic tone. Above conditions revert with ATT therapy and hence ECG abnormalities also disappear.
Possible explanation for persistence of ECG abnormalities is attributed to positional disturbances of heart and mediastinum secondary to pulmonary fibrosis in extensive diseases.

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AIM: To study level of serum concentration of C-reactive protein (CRP) and lipids in patients of acute ischemic stroke and to ascertain the role of CRP levels and its correlation with lipids.

MATERIALS AND METHODS: The study was done during the period of November 2003 to November 2005. Thirty cases (M-18; F-12) were studied taking into consideration exclusion criteria. Detailed clinical histories including family history, personal history, risk factors, treatment history were taken which included detailed general and systemic examination. Routine investigation like Hb, DC, TLC, ESR, S. Urea, S. Creatinine, FBS, Urine: Routine and Microscopic were done. CT scan of brain was done in all cases. Quantitative estimation of CRP by latex fixation technique was estimated. Lipid profile of all cases was done which included estimation of total serum cholesterol (Enzymatic method), HDL cholesterol (Phosphotungstate method), Serum triglycerides (Colorimetric method), LDL-C & VLDL-C (Indirect method by Friedrich’s equation).

OBSERVATION: Raised CRP and levels of lipids were observed as follows:
Age (in Years) Male Female Total (n=30)
No. of Cases Mean No. of Cases Mean
40-50 5 8.42 2 8.3 8.38
51-60 7 8.3 6 8.4
61-70 4 8.45 3 8.67
71-80 2 8.1 1 8.8
Mean 8.3 Mean 8.5
Raised CRP levels were seen in all cases. In all cases lipids showed normal level except LDL which was slightly raised as suggested by Mean Cholesterol-185mg%, Mean TG –171.31mg%, Mean HDL 47.34mg%,Mean LDL 107.32mg%, Mean VLDL 34.26mg%.

DISCUSSION: Out of 30 patients of CT proven ischemic stroke patients all were with raised CRP (Mean 8.38) but lipid profile was not significantly altered except LDL.

CONCLUSION: CRP level was increased in acute ischemic stroke due to inflammatory process. Lipid levels did not increase as studied by others. So it was concluded that there is no correlation of increased levels of CRP in acute ischemic stroke along with lipids in our study. But raised CRP has got a definite prognostic significance.

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