MBBS UM (malaya) EXTENDERS

Which style do u like?

From Chedet.co.cc

1. I gave a talk after I was conferred an honorary degree by the International Medical University. I directed a major part of my talk to the new graduates.

2. I explained that medicine is not just a profession, a qualification for earning a good income. It is a vocation, a calling which involves dedication to the job of healing the sick and caring for them.

3. What their qualification confers upon them is not just a degree but as doctors they have been elevated to a special status and endowed with special powers. They would have in them the capacity to inspire confidence and trust in their patient. The confidence and trust are such that people would literally entrust their lives to them, allowing them to cut open their bodies and do things which could kill if done by others.

4. The skill and the power they acquire owe much to the society in which they were brought up and their access to education up to the highest level. Not all human society can do this. A poor society, an unstable society, an uncaring society would not be able to give them even primary education, much less training to become a doctor. The cost borne by the society is high.Whether they get a scholarship or their parents pay for their education, they all owe a debt to society. It behoves them to repay to society through the service in which they are trained.

5. They should therefore be ready to offer their services to the society in which they lived. It may be by serving the Government or if this is not attractive enough, at least their country. They can earn a good income in Malaysia's private sector.

6. But some easily forget their debt and are easily enticed by higher pay in other countries. These countries paid nothing for their education and training and yet for a little bit more money they get the services of the people we paid a lot to train whether in Government school and universities or in private ones. Quite often the countries which get the service of our doctors are developed and rich.

7. The nation loses a lot when the people we train opts to work in other countries.

8. But the association of doctors make matters worse by refusing entry to foreign doctors to practice. It wants to keep the opportunities for making money in this country to its members only. It does not mind Malaysian doctors going out but foreign doctors may not come in. Only if they work with the Government can they come in.

9. The flow is one-way. Our doctors can leave the country but foreign doctors cannot replace them. We are losing the brains that we develop without the foreign brain coming in.

10. Despite all the Government's efforts we are losing especially the much-needed specialists.

11. There is something wrong here. If the Malaysian Medical Association (MMA) wishes to close the country to outsiders then it should also object to Malaysian doctors from leaving the country. As it is the MMA seem to be wanting to have their cake and to eating it as well.

12. I am not suggesting that as we have embraced globalisation and the free flow of capital etc that we should now allow foreign doctors to come and open their hospitals here. But I do think that if local hospitals need to employ foreign doctors then they should be allowed to.

Some of my batch gone to Singapore, and most of them are the best students in the faculty.

Of coz we can blame them just because gov has support their education eventhough they only apply loan (ptptn), but still of fee about RM1800/year (RM9000)is the cheapest fee to produce a doctor compare to the private medical school which nearly cost RM200,000. But do they care eventhough they were using 'rakyat' money ?

We are currently shortage of doctor, overall a doctor to patient ratio is about 1:1,145. Tan Sri Ismail Merican, director of health said in 2012 the ratio would be 1:600.

Calculation numbers of HOs:

Currently my batch 170. Those who go to singapore are about 10+, those who fail including me are 21 students. That doesn't include pass but then quit medicine which i think less than 5 students. So how much/percentage of doctors currently practice in GOV hospital? - about 75% only! I don't know other university, but i assume it's the same. Can we get our target of 1:600?

I do agree that some of them are too arrogant but can we blame them just because they are not practicing in Malaysia? We cant totally blame them. Working in gov hospital is like working in HELL although we've not been there, yet. Some said doctors should do charity, helping people, bla bla bla etc. Of coz we are helping ppl, but in the end what we get?

Scolded by the patients?
Almost all not appreciate what doctors do?
Low salary?
On Call 3 times/week?
No time for luxury/entertainment/family?
Working like in a factory with polluted air?
Sweating even at night because there is no air-cond?
Lost 5Kgs every months because too busy and forgot to eat?
Getting HIV because of needle prick?

I also do agree on the other hand, most of the doctors are certainly very loyal to the Gov hosp. But try asking them, do they willing to work at gov for the rest of their life if nothing change? Some of them even lost hope to Malaysian Gov, which are just waiting their bond to finish.

Practice in singapore, with only 4 night shifts/months, Salary of $3000++ --> convert RM7000 (eventhough they said they live in singapore the cost of living is high, bullshit i said to them. Do they have savings? They might have about $1000 then later come back to Malaysia once a month and blanje sakan! waaa ternganga mulut aku...) comparing to Gov hosp here basic RM2500. So basically can get about RM 3500++. RM7000-3500 = 3500.. So u actually need to work 4 times harder here to earn that singapore money.. This is HO u know.. Not a MO, Specialist, or Consultant.

So think again, by going to singapore, eventhough we feels like rakyat have been betrayed, whatever u tried to label them such as mata duitan, tak kenang budi, tak semangat patriotik, lupe daratan, selfish doctor, etc, do they care after a lot of benefits and privilege they got. Adding summore, there is no law to prevent them working outside of the country

Of coz malaysia cant support their salary to be as good as our neighbour to prevent loss, but we certainly can put an act. This law should be strict and if ever broken, immediate action such as terminate their license to practice or the worst the university should take back their degree.

What can i said is, Malaysia need a new hope. That's all. If the BN can't do it, who else can do it? PR? such a loser..

5 juta rakyat Malaysia akan dijangkiti H1N1

BUKIT MERTAJAM 15 Ogos — Pertubuhan Kesihatan Sedunia (WHO) menganggarkan lima juta atau 20 peratus rakyat negara ini berisiko dijangkiti virus selesema babi atau influenza A (H1N1) jika langkah pencegahan tidak diambil secara serius oleh orang ramai.

Menteri Kesihatan, Datuk Seri Liow Tiong Lai berkata, kajian WHO juga menjangkakan penularan wabak itu mungkin berlarutan antara enam bulan hingga setahun lagi.

“Kajian itu menyebut bahawa jika penularan virus H1N1 di sesebuah negara tidak berjaya ditangani dengan berkesan, 20 peratus penduduknya akan terdedah dengan jangkitan virus itu,” katanya kepada pemberita selepas melawat Hospital Bukit Mertajam di sini hari ini.

- BERNAMA

Clinico-pathological Conference, 14th August 2009

A 23-year-old man was admitted to the hospital because of complex partial seizures that had become generalized.

The patient, who was from El Salvador, had been well until the age of 15 years, when he had three seizures during a two-month period. He was told that the seizures were caused by a "parasite." A medication, which has not been identified, was prescribed, and there was no recurrence. At the age of 16 years, he had a series of episodes of "panic," each lasting as long as three days. Soon after these episodes, he emigrated to the United States after a four-week stay in Mexico. Ten months later, a tonic–clonic seizure occurred.

The patient was evaluated at this hospital at the age of 17 years. The results of neurologic and hematologic examinations, blood chemical analyses, and screening of the serum for toxic substances were negative; radiographs of the chest were normal. Computed tomographic (CT) scanning of the brain, performed without the administration of contrast material, revealed a focal area of dense calcification, less than 1 cm in diameter, in the region of the left hippocampus, adjacent to the choroid fissure. A lumbar puncture was performed (Table 1). An electroencephalogram was normal while the patient was awake and while he was asleep. Treatment with phenytoin was begun, but the patient discontinued it because of anorexia. A seizure occurred, and carbamazepine was administered.



One year later, another cranial CT study, performed before and after the intravenous administration of contrast material, showed no change in the calcific lesion in the left temporal lobe. A tuberculin skin test (purified protein derivative, 5 TU) was positive, producing a 13-mm induration. A serologic test for cryptococcal antigen was negative. Microscopical examination of a stool specimen revealed giardia. A test for antinuclear antibodies and serologic tests for histoplasmosis, blastomycosis, and coccidioidomycosis were negative. Metronidazole was prescribed. A serologic test for paragonimiasis was negative. Another electroencephalogram was normal, both while the patient was awake and while he was asleep. Radiographs of the chest remained normal. Isoniazid, rifampin, and pyridoxine were administered. The patient was subsequently lost to follow-up for five years.

At the age of 23 years, the patient returned to this hospital. He reported that his seizures had begun when he was 15 years old, after he had been struck on the right side of the head by his father and had lost consciousness. The seizures were preceded by an aura of warmth on the right side of the head; occasionally, he had brief myoclonic jerks before losing awareness. His brother added that the patient would look to the right and then fall, stiffen, and shake for several minutes. Tongue biting and incontinence accompanied the seizures, which were followed by confusion and sometimes combativeness for as long as 30 minutes. The seizures occurred as often as six times weekly but usually occurred two or three times a week. The patient had had only minor injuries as a result of the falls. He had been taking 200 mg of carbamazepine three times daily, presumably on a regular basis, during the two weeks before this presentation. He also reported having generalized fatigue, malaise, and severe headaches. He was admitted to the Epilepsy Service.

The patient's birth and development had been normal. He did not have a history of encephalitis or febrile convulsions and did not use tobacco, alcohol, or illicit drugs. He was unmarried and, because of his symptoms, was unemployed. He resided with his brother. There was no family history of seizures or other neurologic disease.

The temperature was 36.6°C, the pulse 76, and the respirations 18. The blood pressure was 130/75 mm Hg.

A general physical examination revealed no important abnormalities. On neurologic examination, the patient was fully alert and oriented; his speech was fluent. The retinas were normal. The cranial-nerve functions were intact. Motor strength was 5/5 throughout, with normal bulk and tone. Sensation, tendon reflexes, coordination, stance, and gait were normal.

The urine was normal. Hematologic and blood chemical tests (Table 2) and a lumbar puncture (Table 1) were performed. Magnetic resonance imaging (MRI) of the head, performed without the use of contrast material, showed a focus of abnormal magnetic susceptibility in the medial portion of the left temporal lobe, as well as mucosal thickening in the right sphenoid and ethmoid sinuses. Radiographs of the chest were normal. A CT scan of the brain, obtained without the administration of contrast material, revealed a calcific lesion within the tip of the left temporal lobe (Figure 1). A positron-emission tomographic (PET) study of the brain, performed after the intravenous injection of 18F-fluorodeoxyglucose, showed reduced accumulation in the left temporal lobe. No evidence of abnormal 18F-fluorodeoxyglucose uptake was observed elsewhere in the brain.




The dose of carbamazepine was reduced, and then the drug was withdrawn. Continuous video electroencephalographic monitoring for a period of five days showed six typical seizures, each of which was characterized by an initial spike, followed by rhythmic activity in the left temporal region; interictal epileptiform discharges were recorded in a similar pattern. There was no obvious background abnormality in the left temporal region.

Carbamazepine therapy was resumed at the usual dose, and the patient was discharged on the sixth hospital day. He subsequently had one or two seizures per week.

A diagnostic procedure was performed.


Neuroimaging studies were performed over a period of several years. On the CT scan of the head that was obtained on admission to the Epilepsy Service, the only abnormality is a high-density, apparently calcified focus in the medial portion of the left temporal lobe (Figure 1). The lesion appears to be unchanged from that seen on the previous CT scan. On the T2-weighted images from the MRI studies, there is a focus of hypointensity in the same region, which is consistent with the presence of calcification.

Team also performed a pulse-sequence study with sensitivity to magnetic susceptibility in order to help differentiate between the presence of blood products and calcification. The focus of hypointensity did not appear to be enlarged on the pulse-sequence study, a finding that confirmed its calcific nature. On the coronal T1-weighted image, the calcification appeared to be near or within the left choroid fissure.

Before we discuss the differential diagnosis of this lesion, we must decide whether it caused the patient's epilepsy. The first step in localizing the focus of a seizure is to take a detailed history. We have also learned, however, that clinical findings do not always pinpoint the site of a seizure, since many common manifestations of seizures reflect spread of the electrical discharge from a clinically silent cortical area. In the present case, the usual warning was a sensation of warmth on the right side of the head. Unilateral sensory phenomena (with the exception of head pain) reliably indicate a site in the contralateral hemisphere. One cannot assume, however, that within that hemisphere the seizure arose in the primary sensory cortex of the postcentral gyrus; it may instead have spread to that region from the temporal lobe or elsewhere. Even areas outside the parietal lobe, such as the second sensory area of the frontal operculum, can generate such somatosensory phenomena.

When a partial seizure begins to generalize, deviation of the head and eyes toward the right — as reported in this case — suggests that the seizure originated in the left hemisphere (although when temporal-lobe seizures do not become generalized, the head usually turns toward the side of onset of the seizure). Seizures arising from the medial temporal lobe are commonly associated with a visceral, cognitive, or psychic aura and with oral movements after loss of consciousness. Such features did not accompany this patient's seizures. Furthermore, there was no reliable history of isolated simple partial or complex partial seizures, which are almost always more frequent than secondarily generalized seizures in cases of epilepsy involving the medial temporal lobe. It is possible, however, that the patient and those around him did not remember the more subtle events.

In the hospital, the withdrawal of medication would have made secondary generalization more rapid and frequent, possibly masking the early features of the seizures. The prolonged episodes of panic that occurred several years before the current admission could have been a manifestation of simple partial seizures, but a duration of two to three days would suggest simple partial status epilepticus, a very rare condition. Furthermore, the panic did not immediately precede loss of awareness, which would be expected in the case of a true epileptic aura.

In the absence of definitive phenomenologic data, we must rely on ancillary testing, primarily electroencephalographic studies. Localization of both ictal and interictal abnormalities to the left temporal region is very helpful, and if clinical findings suggest involvement of the left hemisphere, the likelihood of a focus in the left temporal lobe is high. The presence of glucose hypometabolism in the left temporal lobe on PET, which is seen in 70 to 80 percent of patients with temporal-lobe epilepsy who have undergone surgery, also supports the possibility of a focus in the left temporal lobe. For these reasons, the calcification seen in the left medial temporal region on the MRI and CT scans is probably of causative importance. Finally, one should not be dissuaded by the small size of the lesion; even very small lesions can cause intractable epilepsy.

Causes of cerebral calcification

Cerebral calcification can have a metabolic, neoplastic, vascular, congenital or developmental, traumatic, or infectious or noninfectious inflammatory cause.

Metabolic processes, such as hypoparathyroidism and other disorders of calcium and phosphorus metabolism, can result in bilateral calcification, which typically involves the basal ganglia and can therefore be dismissed from further consideration. The same is true of other systemic diseases that are occasionally associated with cerebral calcification, such as systemic lupus erythematosus.13

A neoplasm of low-grade malignancy must be carefully considered in this case. Tumors that are found during surgery for chronic epilepsy often lack radiologic characteristics that are typical of other tumors, including edema, mass effect, and contrast enhancement. Furthermore, their radiologic appearance does not change over the course of many years. The types of tumor identified on pathological examination include low-grade astrocytomas, oligodendrogliomas, gangliogliomas, and the more recently recognized dysembryoplastic neuroepithelial tumors. Calcification can be a manifestation of any of these tumors, especially on CT scans, but on MRI scans they typically appear as heterogeneous masses rather than as a uniform focus of calcification, such as that seen in the case under discussion.

Vascular lesions that may give rise to epilepsy include infarcts, primary intracerebral hemorrhages, and congenital vascular anomalies. This patient's history rules out all but the last category, which comprises arteriovenous malformations, venous angiomas, capillary telangiectasias, and cavernous angiomas. Arteriovenous malformations consist of anomalous vessels that have the characteristics of both arteries and veins, with intervening parenchymal tissue, and that are visible on MRI or conventional angiography; MRI scans characteristically show multiple flow voids. Since these features are not present in the case under discussion, an arteriovenous malformation is unlikely, although a small, thrombosed malformation cannot be ruled out. Magnetic-susceptibility studies are helpful in cases in which vascular lesions are suspected.

Venous angiomas have a linear or radial appearance and typically do not cause seizures or calcify. Capillary telangiectasias usually appear in the brain stem and do not cause seizures. Cavernous angiomas are present in about 0.5 percent of the general population and are frequently associated with epilepsy when they are symptomatic. The lesions are characteristically heterogeneous and do not appear as a solid, calcified focus; typically, there is a hyperintense center with a hypointense rim, corresponding to the presence of hemoglobin-breakdown products from previous small, usually asymptomatic hemorrhages. Other surgically important lesions are thrombosed aneurysms of the internal carotid artery or of the circle of Willis, but these are rarely associated with epilepsy and would not be intraparenchymal at a distance from the relevant signal voids on MRI scans. In this case, therefore, the lesion is probably not of vascular origin.

Hamartomas, among other congenital lesions, can appear on CT scans as isolated, nonenhancing foci of calcification. On MRI scans, however, they usually are associated with anomalies now recognized as areas of dysplastic cortex.

Traumatic lesions rarely calcify, and when they do, the calcification is generally seen in an area of bleeding associated with a cerebral contusion. The history of head trauma in this case does not strongly suggest such an injury, and the density of the calcification and the absence of associated encephalomalacia make this an unlikely explanation for the lesion. Cranial irradiation is another form of trauma that can lead to cerebral calcification, but there was no history of it in this case.

With respect to possible infectious or noninfectious inflammatory causes of the calcified lesion, the patient's fatigue, malaise, and headache at the time of the third presentation at this hospital raise the possibility of an active infection, although infection of the central nervous system is improbable, since the cerebrospinal fluid was normal and the lesion had been stable for many years. Among specific causes, viral, bacterial, mycobacterial, or parasitic infections merit consideration.

Multiple areas of calcification may develop after neonatal herpes or cytomegalovirus encephalitis, and a single case of an isolated, calcified temporal-lobe focus in an adult who had had herpes encephalitis has been reported. The history in the present case, however, does not suggest either of these viral diagnoses. There is also no clinical evidence of syphilis, which would be associated with abnormal findings in the cerebrospinal fluid and a positive serologic test, or any other bacterial process.

The possibility of a mycobacterial lesion, however, merits serious consideration. The patient's positive tuberculin skin test indicates that he was exposed to tuberculosis, but positive tests are common among immigrants from developing countries and do not necessarily indicate the presence of symptomatic disease either at the time of the evaluation or in the past. The long course of the patient's illness and the absence of abnormal findings in the cerebrospinal fluid eliminate tuberculous meningitis from consideration. Although isolated tuberculomas can occur, usually they are more than 2 cm in diameter and are enhanced with the use of contrast material, and they rarely calcify. Other granulomatous diseases, such as sarcoidosis, are also unlikely, given the normal cerebrospinal fluid and the absence of contrast enhancement.

Toxoplasmosis is a common parasitic disease that often results in cerebral calcification when it occurs in newborns, but there are almost always multiple calcified foci. In older children and adults, cerebral infection is usually associated with immunosuppressive disorders, particularly the acquired immunodeficiency syndrome. The lesions in those cases, however, are frequently multiple and usually enhance, and the clinical course is much shorter than that in the present case. Trematodes such as schistosoma and paragonimus, both of which are found in Asia and Africa rather than Central America, may infect the cerebrum but typically also invade other organs, such as the liver or lungs, and usually cause seizures only in the acute stage of the disease. Giardia, a common intestinal parasite in developing countries, was found in this patient, but this organism does not cause cerebral infection.

Cysticercosis may be the most common cause of symptomatic epilepsy in the world. The disease is caused by the larval form of the pork tapeworm, Taenia solium, and is endemic in much of Central America and South America, as well as Asia. It is associated with poor sanitation and is acquired through consumption of infected food or by fecal-to-oral transmission. The infected food may be pork, but more commonly transmission occurs through consumption of fruits and vegetables grown in soil fertilized with contaminated pig or human waste.

T. solium is the only tapeworm for which humans can be both the intermediate host, harboring the larval form of the worm, and the definitive host, harboring the adult form. The embryos, or oncospheres, are ingested and absorbed through the intestinal blood vessels into the venous circulation. They pass through the lungs and then embolize systemically, ultimately lodging in skeletal muscle, the eyes, and the central nervous system. In the central nervous system, the oncospheres may lodge in the gray matter, at the junction of the gray and white matter, or in the subarachnoid space. In tissue, the embryos develop into encapsulated larval forms called cysticerci, which are filled with clear fluid and contain a viable scolex. When contaminated meat is ingested by humans, the cysticerci may attach to the intestinal mucosa and develop into mature tapeworms 2 to 8 m in length. The worms are composed of hundreds of proglottids, each of which contains oncospheres that repeat the cycle when the proglottid is shed in feces.

Cerebral lesions typically evolve from an active to a transitional form and then to an inactive form. On CT or MRI scans, the active form appears as a thin-walled, fluid-filled cyst with a mural nodule (the live scolex); it causes no inflammatory reaction. The transitional form is a more proteinaceous, encapsulated cyst with ring enhancement; this cyst becomes a granulomatous, irregularly enhancing lesion as the organism dies. The inactive lesion contains the dead organism and is densely calcified, with no enhancement. At any of these stages there may be multiple lesions, but often the lesions are solitary. Seizures are the most common clinical manifestation at all stages of intraparenchymal infestation, although headaches and focal symptoms are common during the active and transitional stages. Meningeal and intraventricular cysts can result in hydrocephalus.

Solitary areas of calcification are usually supratentorial and less than 1 cm in diameter, without a mass effect, as in the case under discussion; lesions located in the hippocampus have been reported. The negative results on serologic testing in this case do not rule out cysticercosis. Indeed, when inflammation is absent, even the most accurate test, the enzyme-linked immunotransfer blot, is negative in 60 to 80 percent of cases and probably in more than 80 percent of cases involving only a single lesion. Treatment with the antihelminthic drug praziquantel or albendazole may be beneficial during the active and transitional stages of neurocysticercosis and may even help control seizures, but this type of treatment is unlikely to be effective when the disease is inactive.

I believe that the diagnostic procedure in this case was resection of the calcified lesion in the left medial temporal lobe, along with tissue from the adjacent anterior hippocampus and amygdala. When epilepsy results from a solitary lesion, seizure control depends mainly on complete resection of the lesion; whether electrically active tissue should also be removed is controversial. The pathological examination probably showed a degenerated cysticercus organism surrounded by gliosis, without appreciable inflammation. A less likely finding would be a small, thrombosed arteriovenous malformation, a cavernous angioma, or a low-grade astrocytoma. Control of the patient's seizures should be markedly improved as a result of the surgical procedure.

Clinical Diagnosis

Neurocysticercosis, with epilepsy.

Neurocysticercosis, inactive, with temporal-lobe epilepsy.


Pathological Discussion

The patient underwent a left temporal craniotomy. Three fragments of brain tissue were obtained from the junction of the hippocampus and the amygdala. The largest fragment was 3.5 by 2.3 by 1.7 cm. Two of these fragments were grossly normal, but the third contained a round, firm nodule, 3.0 mm in diameter, filled with granular, tan–yellow material and surrounded by a capsule and attached parenchyma.

Histopathological examination revealed a cyst (Figure 2) that was circumscribed by a collagenous capsule, 0.2 mm thick, and attached to a portion of the hippocampus. The lumen of the cyst contained acellular, eosinophilic debris (Figure 3), with scattered, round, basophilic concretions, as well as a dense, homogeneous, refractile cuticle that was serpentine in shape and that rested on a less dense but thicker layer studded with calcified particles. Beneath the second layer were spaces containing debris. The serpentine fragment was probably the remnant of a desiccated scolex, although it was not possible to confirm the identification of the parasite.


A dense, lymphoplasmacytic infiltrate that included rare eosinophils, macrophages containing hemosiderin, and Russell bodies involved the capsule (Figure 4) and the parenchymal vessels (Figure 5).


The portion of the hippocampus near the capsule was gliotic, with focal neuronal loss (Figure 6). Some of the remaining neurons were encrusted with granular, ferruginous material. There were also foci of perivascular or vascular chronic inflammation.


These findings are consistent with a diagnosis of cysticercosis involving the cerebrum, with features that are characteristically observed 2 to 10 years or even longer after infestation.33 The central nervous system is involved in 90 percent of cases of human cysticercosis.34 The presence of a single cerebral cysticercus in this case is unusual, however, since in 80 percent of the cases multiple cysts are found.35

Four types of central nervous system cysts are encountered in cysticercosis. Parenchymal cysts are usually found in the cerebral cortex, including the cortical–subcortical junction; the white matter is rarely involved. Meningeal cysts form in the meninges overlying the base of the brain more often than in the meninges overlying the convex surface, sometimes causing hydrocephalus and strokes. Ventricular cysts are usually located in the fourth ventricle and cause intermittent hydrocephalus and, occasionally, sudden death. Spinal cord cysts are rare.

The host can tolerate the worm as long as the embryo is alive. It usually dies two to six years after infection, and the ensuing disintegration of the parasite triggers a vigorous tissue reaction. The dead parasite eventually decays into grumose or eosinophilic, desiccated material. The final stage of this process is characterized by the presence of a calcified nodule, presumably the result of dystrophic calcification of the necrotic larva.

Small Talk

The patient has been free of seizures since his left temporal lobectomy.

If the development of seizures is related to an inflammatory process, how does it increase excitability?

The mechanism is not known, but one hypothesis is that the lesion disturbs the microenvironment of the surrounding neurons, either by affecting neurotransmitters or by stimulating axonal reorganization in ways that favor excitation over inhibition. Inflammation does not always accompany the lesions that cause seizures, however.

Does the sensitivity of serologic testing change over time?

Several studies suggest that the sensitivity of serologic testing decreases considerably late in the course of the disease, especially when only a single lesion is present.

Anatomical Diagnoses

Neurocysticercosis, left temporal lobe, end-stage, with calcification.

Epilepsy.


Death Certificate

Will continue adding later



References
CPC Faculty of Medicine, University of Malaya
http://content.nejm.org/cgi/content/full/343/6/420
http://www.neurology.org/cgi/content/full/57/2/177

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Baru blaja, of coz la maybe one of u said sikit.. but hey, lama2 jadi bukit ape.. infact, no one will wanna give u easy2 RM71 what... Cant wait for raffiq turns to get money






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1 YAY.. DUIT NUFFNANG DA DAPAT!!!!
2 Claiming Nuffnang Money

This post is a follow up on a case which i discuss earlier. In case if you wanna know a bit about the patient history or you are lost, care to click here.

Patient currently on week 2 and currently on day 4 of oral augmentin course change from previous IV augmentin due to development of rashes based on Prof MT Koh saying that the cause of the rashes which raised on the patient trunk and the limbs could be from the antibiotic given. I'm start to think, patient was already on IV augmentin for 12 days and if the rashes really due to the antibiotics given, shouldn't it comes early? And if the patient really have the rash problem due to antibiotic, is the route of administration of the drug makes the rash goes away eventhough it using the same antibiotics? but anyway, the rashes was still there for the past 3 days.

Currently, oncology team lead by Prof MT Koh, makes the working diagnosis as Haemophagocytic Lymphohistiocytosis, which is a rare disorder of the immune system. The disease clinically manifests as fever, hepatosplenomegaly, pancytopenia(which the patient's platelet is normal), lymphadenopathy, and rash(and no rashes initially) often comprise the initial presentation.


Hemophagocytic Lymphohistiocytosis

The diagnostic criteria set forth by the Histiocyte Society for inclusion in the International Registry for Hemophagocytic Lymphohistiocytosis (HLH) is as follows. All 5 criteria must be met to establish a diagnosis of hemophagocytic lymphohistiocytosis:


* Fever - Seven or more days of a temperature as high as 38.5°C (101.3°F)
* Splenomegaly - A palpable spleen greater than 3 cm below the costal margin
* Cytopenia - Counts below the specified range in at least 2 of the following cell lineages:
o Absolute neutrophils less than 1000/µL
o Platelets less than 100,000/µL
o Hemoglobin less than 9.0 g/dL
* Hypofibrinogenemia or hypertriglyceridemia - (1) Fibrinogen less than 1.5 g/L or levels greater than 3 standard deviations below the age adjusted reference range value or (2) fasting triglycerides greater than 2 mmol/L or levels greater than 3 standard deviations above the age-adjusted reference range value
* Hemophagocytosis - Must have tissue demonstration from lymph node, spleen, or bone marrow without evidence of malignancy
* Rash - Skin findings in more than half of patients;1 scaly and waxy lesions; rashes on the scalp and behind the ear
* Other - Swollen or hemorrhagic gums that can result in tooth loss; feeding problems (especially prominent in infants); abdominal pain, vomiting, diarrhea, and weight loss




Discussion

I don't know why they were searching for all those rare things. If i answer this HLH in my long case final exam, sure GG. They are currently planning to have some blood investigations to confirm the HLH by doing fasting TG, fibrinogen, and waiting for trephine report.



When i ask one of the doctor there, why would they haven't done their lymphnode biopsy, the answer somewhat like this

"This is a generalised lymphadenopathy. How could we biopsy all the lymphnodes?????"

I don't know wether its true or not, but currently there is no plan for lymphnode biopsy yet.

A big suprise where today was the first time the patient is 24 hour free from fever. Maybe an oral antibiotic is working after all..

Today i've managed to present one case of a 4 year old child with fever for 4 weeks with no other clinical symptom except loss of appetite, lost of wt of 1 kg and a bit lethargic and less active. There was no RTI, GIT, CNS symptom. Fever was reduce by antibiotics. No night sweat. Then later was referred from a GP due to fever and palpable cervical lymphnodes. Got a history contact to TB patient(grandmother). Vaccination was complete.

Physical examination reveals fever, palor, with hepatomegally (1cm) and generalised lymphadenopathy. No bcg scar noted


So differentials would be
1) Tuberculosis
Points favour - History contact with TB, loss of wt and appetite. PE reveals fever, palor, hepatospleenomegally and also generalised lymphadenopathy and no BCG scar.
points agains - No cough, haemoptysis, and night sweat.

2) Leukaemia
Points favour - Lethargy, fever, palor, hepatomegally, lymphadenopathy
Points against - No bleeding tendency, no family history of blood malignancy, no spleenomegaly

3) Lymphoma
Points favour - B symptom? (must really need to clarify is there any night sweat because patient was in an aircond when sleeping) and also lymphadenopathy
Points agains - i couldn't think of... maybe u can give me a comment

4) HIV - fever
points against - No hx of blood transfusion,

5) Thyphoid/thyphus
Points favour - PUO, lymphadenopathy, hepatomegally
Points against - no spleenomegally, no

6) autoimmune? connective tissue disease?


Investigation that was done and some I think should be done base on the differentials given are:

1)FBC
Investigation fbc reveals hb low, white cell low, but platelet and wcc differentials are normal.

2)PBF shows normocytic and normochromic anaemia. No blast cell seen

3)Mantoux test
negative

4)Chest xray
No mediastinal lmphadenopathy noted.

5)Bone marrow film
No abnormal/malignant cell noted. Comment said that we should look for viral causes.

6)Lymphnode biopsy
Not done yet

7) HIV screening (permission should be taken 1st when doing HIV screen), Hepatitis screening
-ve

8) Toxoplasmosis?
No plan yet for this toxoplasma screen

9) Infectious Mononucleosis??

10) Blood culture
-ve for all bacteria, virus,

11) Thyphoid/Thyphus
-ve

12)



Diagnosis

PUO and currently on investigation.


Comment

Currently, patient on IV antibiotics, fever are up and down, and relief with PCM. Antibiotics given shown to have positive result, but they are trying to off it to let see if the fever spike up again.

Platelet count was normal despite HB and WBC low. wbc was low until 2 and this is what we call febrile neutropaenia. Prof Amir has said that if a patient come with febrile neutropaenia, we should do a septic screen (blood culture, urine culture, oral swab etc..). However all the test was negative.

Mantoux test was negative however it doesn't mean that the diagnosis should be exclude. there was no BCG scar showing that

Bone marrow was also negative of malignant cell, however, if the bone marrow is negative we can do a lymph node biopsy. Correct me if I'm wrong.



I will follow-up the patient progress and post it on here later. Anything in mind can contact me. Thanks in advance.

Mama called just now.. she said that someone sent me a check! I ask, how much? she said RM71! lolz.. This must be nuffnang. For your info, i've applied it 27th June and they send it at 6th June!! wow.. That's FAST! I was a bit shock when this current situation where economy is turning down, they still paying!

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If u haven't register at nuffnang, now is the time for u to apply it! it's not a scam. Later I'll post my check for u guys to see the proof. but anyway, there's a lot of evidence where nuffnang is paying. Just google it!

Thanks NUFFNANG... i'll used that money to blanje makan to my group members.

Ibu baru bersalin korban pertama di Sarawak

KUALA LUMPUR 3 Ogos - Seorang wanita berusia 23 tahun yang baru dua minggu bersalin menjadi korban ketujuh virus selesema babi atau influenza A (H1N1) di negara ini.

Mangsa merupakan kes kematian pertama H1N1 di Sarawak.

Ketua Pengarah Kesihatan, Tan Sri Dr. Mohd. Ismail Merican berkata, mangsa meninggal dunia pada pukul 4 pagi ini setelah dimasukkan ke Unit Rawatan Rapi (ICU), Hospital Miri, Sarawak sejak 22 Julai lalu.

''Dia dimasukkan ke ICU kerana mengalami komplikasi pada paru-paru dan disahkan dijangkiti H1N1 pada 23 Julai lalu. Dia telah bersalin di hospital sama dua hari sebelum itu,'' katanya dalam kenyataan di sini hari ini.

Beliau berkata, wanita itu didapati menghidap pneumonia yang teruk selepas bersalin selain mengalami simptom demam dan batuk empat hari sebelum bersalin.

''Bayi wanita itu didapati selamat dan disahkan bebas daripada H1N1. Penyebab kematian direkodkan sebagai pneumonia akibat jangkitan H1N1,'' jelas beliau.

Mohd. Ismail menambah, sebanyak 17 kes baru H1N1 termasuk satu kes kematian dilaporkan di negara ini menjadikan jumlah kes terkumpul H1N1 meningkat kepada 1,446 kes.

''Kesemua kes baru itu adalah jangkitan tempatan yang melibatkan rakyat Malaysia. Jumlah kematian akibat H1N1 di negara ini setakat ini adalah sebanyak tujuh orang,'' katanya.

Menurutnya, daripada 1,446 kes terkumpul H1N1, sebanyak 574 merupakan kes import dan 872 adalah kes jangkitan tempatan.

''Daripada jumlah ini, 1,408 kes telah sembuh, hanya 29 kes sahaja yang sedang menerima rawatan antiviral di hospital yang mana lapan daripadanya berada di ICU. Sembilan orang sedang menerima rawatan antiviral di rumah,'' katanya.

Beliau berkata, daripada lapan kes di ICU, empat daripada mereka mempunyai faktor risiko iaitu obesiti (1), wanita hamil (1) dan imuniti rendah (2).

Mohd. Ismail berkata, bagi 17 kes terpencil, tujuh kes dirawat di wad pengasingan hospital, satu kes di ICU dan sembilan orang menerima rawatan pesakit luar.

Merujuk kepada situasi global sehingga hari ini, beliau memberitahu, sejumlah 183,854 kes H1N1 dengan 1,307 kematian telah dilaporkan daripada 167 negara.

''Ia melibatkan peningkatan sebanyak 28 kes termasuk enam kes kematian berbanding dengan hari sebelumnya,'' katanya.

Beliau berkata, orang ramai yang mempunyai gejala jangkitan H1N1 berterusan dan bertambah teruk disaran mendapatkan rawatan di klinik serta hospital yang berdekatan.

''Kes-kes yang mempunyai simptom jangkitan influenza serta faktor risiko seperti mengandung, obesiti, asma, penyakit paru-paru kronik, diabetes dan golongan imuniti rendah akan diberi rawatan antiviral influenza serta-merta tanpa perlu membuat ujian pengesahan H1N1.

''Ini adalah untuk kes-kes yang dikesan dalam masa 48 jam selepas mereka mula mengalami simptom jangkitan influenza. Ujian pengesahan jangkitan influenza hanya perlu untuk kes-kes yang dirawat di hospital,'' katanya.

1) Today started my new posting - paediatric. Prof Asma was very critical to our history taking and i managed to get something from her class today this morning.

2) Although the first case was very simple, a respiratory infection, it seems that there are a lot we still don't know.

3) The way we should took a history is to let the patient tell the event from the beginning until the end without us interrupting in the middle.

4) After the patient finish talking, then we clarify the gaps and take further history which are relevant.

5) English, again are very important, enough say.

6) We don't create a history. Read back what we took. Is the history was really a logic event? If it not, clarify again with the patient.

7) Prior to admission, is the 'key' date. In the mean while, we can also use the 'day of illness' for associated symptom. How many days did the patient has admitted is also an important history.

8) 4C's should be in the history - chief complain, causes, complication, and course of the disease. Thus we really need to know how was the patient progress.

9) Current situation such we're having now - H1N1 should bear in our mind now.

10) The 2nd case is a dengue haemorrhagic fever.

11) I should admit it, this was the first time i saw the rashes like the patient had. If Prof Asma don't tell me it's rashes, i wont know.

12) The last time i saw a dengue rashes was a bit different from this. I should see and identify a lot of different presentations of dengue rashes.

13) There was 3 other differentials based on history - acute glomerulonephritis, hepatitis, and urinary tract infection.

14) Investigation that has been done are FBC - to see the platelet level, haematocrit, UFEME. Prof said we need to exclude the differential also by doing ASOT or ESR.

15) Treat dengue by giving IV maintenance half saline and check for heart rate, resp rate, urine output, and also sign of ascites and pleural effusion.

16) Lastly, thanks Prof Asma. I was hoping my URTI heals faster.