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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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Over the last few decades Coronary artery diseases (CAD) has become one of the most important causes of morbidity and mortality. Homocysteine is now emerging as an independent modifiable risk factor. Keeping this in mind the present study was undertaken at V.S.S. Medical College & Hospital, Burla in the Department of General Medicine to observe the association of hyperhomocysteinemia as a risk factor in coronary artery disease.


Selection of cases: any patients having evidence of CAD in the form of:
1. Myocardial infarction
2. Stable angina
3. Unstable angina.
Patients having renal diseases, hypothyroidism, SLE, Rh arthritis were excluded from this study. Patients on drugs like methotrexate, phenytoin, biguanides were also not included. 50 cases studied compared with 30 age sex match controls taken.
All the cases and controls were subjected to detail clinical examination and investigation (Routine blood tests, lipid profile, ECG, Cardiac markers) and serum homocysteine estimation by Chemiluminescence's method. A selected nos. of patients were given Vitamin supplementation (folic acid 400 microgram, B6-3mg, B12 10 microgram) for a period 6 weeks and homocysteine was re-estimated. RESULTS:
50% of patients were in the age group of 45-54 and male: female 35:15.70% of cases found to having AMI, 18% having stable angina and 12% having unstable angina. The serum Homocysteine level was found to be high in 60% of cases. (71.42% in male and 33.33 % in female). The Homocysteine level was predominantly high in younger age group. After 6 weeks of Vitamin supplementation mean homocysteine was found to be decreased to significant level (before treatment mean homocysteine level was 20.11 micro mol/L and after treatment 14.06 micromol/L.
The high Homocysteine level is associated with risk of CAD and it is more marked in younger age group and in male sex. Although results of ongoing studies of impact of vitamin-B supplementation on mortality reduction, not available, plasma homocysteine level reduction should also be consider as a prophylactic goal to reduce prevalence of CAD.

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To study the clinical profile and prognosis of AMI in diabetics in contrast to AMI in non-diabetics in present era of aggressive management of AMI from Janurary2003 to March 2004.

In present study 35 patients of AMI with diabetes mellitus and 35 patients of AMI without Diabetes mellitus in Department of General Medicine and Department of Cardiology were included. These patients were assessed & followed up in following manner.

All the patients were subjected for detail clinical examination and history at time of presentation to the hospital with special emphasis on particular complication. Serial ECG was done at Zero hour, 12 hour, 24 hour and daily till date of discharge. Routine X-ray was done in all cases to see evidences of pulmonary hypertension and other pathology. Routine biochemical investigations including liquid profile, blood urea, creatinine, glycosylated Hb, cardiac enzymes was done. Detailed Echo examination was done in all cases. All cases were critically evaluated at the time of discharge and were followed up to 30 days.

The clinical course of acute myocardial infraction (AMI) was compared between 35 known diabetics (Ds) and 35 non-diabetics (NDs). AMI patients matched for age, sex and hospital ward. In both groups similar number of cases with shock pulmonary edema and clinical observed arrhythymias were found. In contrast, diabetic patients had significantly more frequent. A-V and intra-ventricular conduction disorder then non-diabetics (P<0.02). Diabetics also died twice more often from AMI (30%) than matched controls (15%) Diabetics with arrhythymias and/or conduction disorders had a particularly poor prognosis for surviving, the relative risk exceeding 3.


The higher mortality and complication of AMI Diabetics calls for aggressive correction of metabolic and modifiable risk factors, treatment of acute events and secondary prevention,

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To study incidence of neuropsychiatric manifestations and post malarial neurological sequelae in patients of falciparum malaria.

Patients with fever and MP (slide, QBC) showing PFR positive were enrolled for this study and detail history, general examination, neurological examination and psychiatric evaluation including mini mental score, routine examination, CT scan of brain were done at the time of admission, during hospital stay, after recovery and during follow up.

Fourty (40) patients were enrolled in this study, of which 32(80%) were male and 8 (20%) female. The clinical presentation at the time of admission was fever (100%), anemia (77.5%), impaired consciousness(32.5%), psychosis (25%), convulsion (17.5%), , hypotension (13%), only 12.5% patients were deeply comatose with GCS score  7, out of which one (1) patient died.During hospital stay, 2.5% patients developed focal neurological deficit 12.5% patients depression, 5% patients speech disorder in the form of dysarthria, 5% patients memory loss & 5% patients developed acute cerebellar syndrome. Mini mental score (MMS) examination of patients after completion of antimalarial treatment revealed two (2) patients with MMS  21 i.e., they were showing cognitive impairment. Heavy parasitemia was observed, particularly in more numbers of patients with coma and depression. High blood urea (> 49 mg%) was seen to be correlated with impaired consciousness, psychosis, depression and memory loss with p value < 0.005. Three (3) of the patients developed post malarial neurological syndrome in the form of psychosis(1), delayed cerebellar ataxia (1) and memory loss (1).

Neuropsychiatric manifestations are important aspects of clinical features of falciparum malaria, because of it unique characteristics leading to micro vascular involvement. Heavy parasitemia and high blood urea were well correlated with most neuropsychiatric manifestations of falciparum malaria which needs further discussion. So proper anti-malarial treatment needs to be instituted promptly to avoid these complications and postmalarial neurological syndrome to a minimum.

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