JIACM 2005; 6(2): 114-21

CLINICAL MEDICINE

Single Small Enhancing Computed Tomography Lesion: A Review

AP Jain*, Rajnish Joshi**, Tejal Lathia***

Abstract
Single small enhancing computed tomography lesion (SSECTL) is a clinico-radiological entity being reported more frequently as
imaging of the brain becomes more prevalent. The main controversy is whether these lesions are tubercular or neurocysticercal.
This article describes a diagnostic approach to SSECTL mainly on clinical and imaging grounds with supportive evidence from
immunologic and epidemiologic factors. Controversies in management of SSECTL are briefly discussed with guidelines based on
clinical course and CT characteristics of the lesion.
Key words: Tuberculoma, Neurocysticercosis, Diagnostic approach.

Introduction of cysticercus or its parts. None of the patients were found

As the imaging of the brain by computed tomography
became more prevalent, many authors, in particular those
from the developing world, reported lesions in the CT of
patients who were undergoing investigation for seizures
(focal or generalised) which were single, small, and
enhanced with contrast injection.
Early radiological studies labelled most of these lesions
as ‘tuberculoma’1. In one of the earlier Indian studies such
lesions were seen in as many as 26% patients undergoing
CT scan to determine the cause of seizures2. Most of these
patients were started on anti-tubercular therapy. It is hard
to disprove that some of these lesions might actually be
intracranial tuberculomas. The circumstantial evidence of
tuberculosis is present in many patients (past history of
active tuberculosis, history of contact, old healed shadows
on chest X-ray, and positive Mantoux test), none of which
is specific for an active disease. Since such multiple lesions
are seen in patients with proven tubercular meningitis, it
was logical to believe such a lesion to be an ‘immature
form of tuberculoma’1.
It was soon realised that some of these lesions
disappeared after anticonvulsant therapy alone without
any specific therapy3. These lesions were termed as
“appearing and disappearing lesions” or “vanishing CT
lesions”, and speculation increased regarding their
probable aetiology4. In a study conducted in 1993, excision
biopsy and histopathological analysis of single small CT
lesions showed that 12 out of 15 patients had evidence
to have neoplasm or tuberculosis5. The authors advised
against arbitrary use of anti-tubercular therapy in such
cases6. Amongst single contrast enhancing lesions on CT
scan, those less than 20 mm were classified as small and
termed “single small enhancing computed tomography
lesion (or SSECTL)7. The criteria for SSECTL included
patients who had acute symptomatic focal seizures with
or without secondary generalisation; minimal or no
neurological deficit; no evidence of raised intracranial
tension, and no evidence of systemic disease8.
Various authors have studied the resolution of SSECTL in
patients without any specific therapy except anti-epileptic
drugs (AED) for symptomatic relief. The percentage of
resolution over a period of 3 - 6 months ranges from 50 -
75%9-12. Use of steroids alone or in combination with
albendazole did not make significant difference to time
to resolution12.
A Thai study13 evaluated 1,000 patients with various seizure
disorders, of whom approximately 10% had seizure and a
solitary lesion. Roughly 80% of patients had lesions more
than 20 mm and were excluded. On follow-up of these
excluded patients (> 20 mm), only 1 had spontaneous
resolution while the rest had persistent lesion on CT. Of the
remaining 20% included in the study, 90% had complete
resolution by 6 months. Of the two patients with persistent
lesions, one underwent excision biopsy which revealed
eosinophilic granuloma. The other patient refused biopsy,
anti-tubercular treatment was prescribed and lesion

* Director-Professor and Head, ** Lecturer, *** Resident, Department of Medicine,

MGIMS, Sewagram, District Wardha, Maharashtra - 442 102.
resolved after 4 months. This study externally validated the Table I: Frequency of signs and symptoms in 753 cases
previously described criteria and calculated the sensitivity of SSECTL26.
and specificity as 95 and 97 per cent respectively with a Symptom Occurrence (%)
negative predictive value of 98 per cent.
Epilepsy 52.4
Thus, the first controversy is whether the majority of such Headache 43.4
lesions are tubercular or neurocysticercal in origin. The Papilloedema 28.0
second controversial issue is whether these lesions are Pyramidal tract signs 27.2
really single. There are reports of single lesions on CT which Intellectual deterioration 21.5
turned out to be multiple on MR imaging. Presence of Ataxic gait 15.8
multiple lesions does increase the suspicion of tubercular Diminution of visual acuity 10.0
aetiology. Since many patients may not return back after Optic atrophy 10.0
a course of anti-parasitic therapy, it would be disastrous if Psychotic episodes 6.5
some of them go on to develop neurotuberculosis. Diplopia 4.7
Vertigo 4.5
Epidemiology Dysmetria or intention tremor 4.1
It is difficult to estimate the community prevalence of Lower cranial nerve palsy (VII to XII) 3.9
SSECTL. The most common methodology has been to Disturbances of behavior 3.4
carry out epilepsy surveys and to carry out imaging Hypoaesthesia 2.7
studies on all patients with history of focal seizures. Decreased hearing 1.8
Estimated community prevalence of SSECTL by this Spinal cord compression 1.4
method has been found to be around 4%, but some other Meningeal irritation signs 1.4
studies mention it to be responsible for half of all partial
Radicular syndrome 1.3
seizures14, 15. A case series of over 2,500 patients from a
Parinaud’s syndrome 1.0
tertiary care centre in South India observed SSECTL as the
provoking factor in 61% of patients with an isolated
Imaging
seizure16.
Computed tomography
The commonest cause of SSECTL is neurocysticercosis,
which is common in societies where wandering pigs are Since SSECTL is a clinico-radiological entity, the diagnostic
seen. Various myths regarding neurocysticercosis need to dilemma begins when either an asymptomatic or
be broken. Firstly it does not occur by eating pork as even symptomatic patient (usually with focal seizures) shows
undercooked pork will cause only intestinal cysticercosis. a characteristic small (< 20 mm) lesion on CT which
Vegetarian food like salad leaves, lettuce, and celery are enhances with contrast. The initial differentiating features
more of a risk especially in areas of open defaecation. are accompanying radiological characteristics of the
Public education and sanitation may be successful in lesion.
eradication of the disease from the developing world17.
The characteristic lesion on a plain CT of
neurocysticercosis is a small high attenuation lesion
Clinical picture surrounded by peri-lesional oedema18. At times, it may
The usual presentation of SSECTL is in the form of focal show only low attenuation lesion depicting focal oedema.
seizures. Raised intracranial tension is seen in a fifth of The lesion enhances with contrast as a ring, disc, or target
them. Focal deficits are seen variably, and diplopia may lesion. The shape may be ovoid, doughnut-like or bi-lobed
result from intracranial hypertension or arachnoiditis in some cases. There is no or minimal mass effect. There is
producing entrapment and compression of cranial nerves no specific site of predilection; however, most of these
III, IV, or VI (see Table I). lesions are situated at the gray-white matter junction19.

Journal, Indian Academy of Clinical Medicine
Vol. 6, No. 2
April-June, 2005 115
These lesions are as a rule smooth and regular in outline.
In a study of biopsy proven lesions, Chandy and
Rajshekhar5 reported that amongst 31 consecutive cases
of ring enhancing lesions (25 of them were cysticerci, and
6 tuberculomas), all cysticercus granulomas were less than
20 mm in size. In comparison, all tuberculomas were
greater than 20 mm in size. Moreover, 96% of cysticerci
had a regular outline with no mass effect or midline shift,
contrasting 5 out of 6 tuberculomas which were irregular
in outline and 4 of 6 had evidence of midline shift on CT.
Presence of calcification, and perifocal edema was seen
in both, and was not a differentiating feature.
Magnetic resonance imaging
MR imaging is another useful tool for the diagnosis and is
far more sensitive than CT scan in picking up parenchymal
lesions in the brain especially in the posterior fossa. Often
what is thought to be a solitary lesion will turn out to be
one of many such lesions, changing the diagnosis
altogether in some cases. The other significant advantage
MRI enjoys over CT is the detection of scolices which are
usually missed on CT. If scolices are picked up, the
diagnosis of neurocysticercosis is clinched, preventing the
patient from undergoing expensive, potentially toxic and
unwanted drug therapy. However, SSECTL represents a
dying parasite and as such, the scolex may have been
destroyed and not visible on the scan20.
Desai and Bhatia21 observed differences in the MRI picture
of tuberculoma and cysticercosis. On T2 weighted
sequences, tuberculomas were seen to lose signal
intensity, while the intensity of cysticerci increased from
first to second echoes. The sensitivity and specificity of
MR imaging in making the aetiological diagnosis of
SSECTL remains to be determined. If available and feasible,
MRI must be undertaken. This is an exorbitant and not
easily available tool putting it out of the reach of most
patients in developing countries who are the ones who
suffer from this disease. These limitations perforce
necessitate a decision on basis of clinical and CT grounds.
Biopsy
Histopathological confirmation of lesion is ideal but due
to sheer prevalence of such a lesion in developing
countries, where such diagnostic facilities are sparse, focus
116 Journal, Indian Academy of Clinical Medicine
has been on less invasive and more easily done
diagnostics. Moreover, in biopsy samples, there remain a
proportion of biopsies where neither the entire
cysticercus nor its parts are found, but the histological
picture is suggestive of a parasitic granuloma.
A study carried out by Chacko et al22 which reviewed a
total of 54 excision biopsies, 50% were cysticerci with
either the entire parasite, its parts, or degenerated forms
visible.15 of these 28 showed intracorporeal vacuoles
(evidence of degenerated parasite) and 40% of these were
calcified. In the remaining patients where no parasitic parts
were seen, no features suggestive of tuberculosis or fungal
disease were seen either. In fact, they all had features
which favoured a parasitic aetiology, namely,
1. a cavitary inflammatory lesion,
2. presence of eosinophils in inflammatory infiltrate,
3. absence of caseous necrosis, and
4. absence of acid-fast bacilli (AFB) or fungal elements.
On a careful search in the original and 5 micrometre
deeper sections, 6 biopsies showed calcified ovoid bodies,
structurally similar to intracorporeal vacuoles, which also
helps in diagnosis of cysticercosis.
However, it needs to be reiterated that the surgical
excision of an SSECTL is neither recommended nor
required in most of the cases, and that pathological
verification is indicated only in enlarging or persistent
lesions. Other diagnostic modalities have a supportive
rather than definitive value.
Immunological tests
Immunological tests for tuberculosis, neurocysticercosis,
or toxoplasmosis have limitations as these organisms are
seen even in normal individuals in most countries of the
developing world. The tuberculin test is of poor diagnostic
use as 40% of the adult population may be positive due
to prior exposure. The results of conventional ELISA for
cysticercus antibodies in serum and CSF of patients with
SSECTL have been generally disappointing (sensitivity of
50% and a specificity of 65%)23. Serological tests are useful
if positive, but negative test results do not rule out the
disease. False positive serology can result from past
infection with Taenia solium or cross reactivity with other

Vol. 6, No. 2
April-June, 2005
helminths24. False negative serology can result because
of immune tolerance, inactive disease, or localised
antibody production in the CSF. The newer enzyme-linked
immunoelectrotransfer blot (EITB) assays on serum or CSF
using purified glycoprotein antigens from T. solium
cysticerci have claimed much higher sensitivity and
specificity of 98% and 100% for multiple active cysts and
extraparenchymal NCC, but sensitivity is less for
calcifications or single cysts, respectively in Latin American
samples25.
Cerebrospinal fluid analysis
It is indicated in patients with new onset seizures, with a
solitary lesion on neuroimaging, unless there is severe
oedema, midline shift, or obstructive hydrocephalus. If
there is associated tubercular meningitis, raised CSF
proteins, normal sugars and lymphocytosis may be seen.
CSF findings in neurocysticercosis include mononuclear
pleocytosis, normal glucose levels, elevated protein levels,
high immunoglobulin G index, and in some cases
presence of oligoclonal bands. Sotelo et al in a study of
753 cases observed that demonstration of eosinophils in
CSF, though not pathognomic, was valuable indirect
evidence of NCC. When CSF was inflammatory, eosinophils
were found in 57.7% of cases. Far less specific, but still
another frequent finding was hypoglycorrhachia detected
in 17.7% of the cases with inflammatory CSF26. The above
findings were absent in non-inflammatory CSF. However,
if the disease is limited to the brain parenchyma, CSF
examination may be normal, as is expected in the majority
of cases of SSECTL.
Clinical presentation and CT scan remain the mainstay of
diagnosis in the developing world. The clinico-radiological
picture forms the basis of diagnostic criteria for benign
SSECTL as proposed by Chandy et al in 19915. All criteria
must be satisfied for a diagnosis of benign SSECTL.
The clinical criteria are:
1. Seizures (partial or generalised) should be the initial
symptom.
2. There should be no features of persistently raised
intracranial pressure.
3. There should be no history of a progressive
neurological deficit.
Journal, Indian Academy of Clinical Medicine
Vol. 6, No. 2
4. There should be no evidence of an active systemic
disease.
The radiological criteria are:
1. CT scan should only show a solitary, contrast-
enhancing lesion.
2. The lesion should measure less than 20 mm in
maximal diameter.
3. Oedema may or may not be present, but is not severe
enough to produce a shift of the midline structures.
These clinico-radiological criteria were found highly
sensitive and specific in predicting benign outcome5. The
diagnostic criteria for neurocysticercosis based on
objective clinical, imaging, immunologic, and
epidemiological data have been proposed by Del Brutto
et al, which in addition to the clinical usefulness, also offers
to bring uniformity in research on SSECTL (See Table II).
Management of SSECTL
The controversy in management persists, especially when
the treating physicians prefer to err in favour of
tuberculosis rather than cysticercosis. Many would
empirically treat both, which has issues related to both –
costs and toxicity of anti-tubercular therapy, which in
neurotuberculosis may vary from six to eighteen months.
Some general rules have been proposed to overcome this
dilemma.
The management algorithm7
Patients who do not have raised ICT, progressive
neurodeficit, ancillary evidence of tuberculosis or
malignancy, should be treated with anti-convulsants only
as 50-75% of patients show spontaneous regression of
lesion on AED’s alone. However, a repeat CT scan would
be required after 3 months if patient is symptom free and
neurological examination is normal. CT may be done
earlier if seizures are uncontrolled or new signs and
symptoms occur.
The further management depends on the CT result:
1. If the lesion is of same size or smaller than baseline,
oedema is less and clinically patient is seizure free,
anticonvulsants are continued.
2. If the lesion shows enlargement, but it is still less than

April-June, 2005 117
 20 mm with no shift or ventricular compression, give
a course of anti-parasitic drugs alongwith the
anticonvulsants.
3. If the lesion is greater than 20 mm in size with
evidence of midline shift or ventricular or gyral
compression, it should be further investigated as only
1 such lesion out of 88 will spontaneously resolve.
Radiological or other ancillary evidence of
tuberculosis is sought.
Lesions which are calcified would need much longer anti-
epileptic therapy, as it represents a healed lesion.
Table II: The diagnostic criteria for neurocysticercosis37.
Criteria
Absolute

Histologic demonstration of parasite from biopsy of
brain or spinal cord lesion.

Cystic lesions showing scolex on CT/MRI.

Direct visualisation of subretinal parasites on
fundoscopic examination.
Major

Lesions highly suggestive of neurocysticercosis on CT/
MRI (neuroimaging studies).

Positive serum immunoblot for the detection of anti-
cysticercal antibodies.

Resolution of intracranial cystic lesions after therapy
with albendazole or praziquantel.

Spontaneous resolution of single small enhancing
lesions.
Minor

Lesions compatible with neurocysticercosis on
neuroimaging studies.

Clinical manifestations suggestive of
neurocysticercosis.

Positive CSF ELISA for detection of anticysticercal
antibodies or cysticercal antigens.

Cysticercosis outside the central nervous system.
Epidemiologic

Evidence of a household contact of T. solium infection.

Individuals coming from or living in an area where
cysticercosis is endemic.

History of frequent travel to disease-endemic area.
Definitive diagnosis: 1absolute criterion; or 2 major, 1 minor, and
1 epidemiologic criteria;
Probable diagnosis: 1 major plus 2 minor criteria; or 1 major, 1
minor, and 1 epidemiologic criteria; or 3 minor and 1 epidemiologic
criteria.
118 Journal, Indian Academy of Clinical Medicine
Do anti-parasitic drugs really help?
The anti-parasitic therapy for neurocysticercosis is not
without controversy. The most contentious issues are dealt
with in Table III. After the initial success of anticysticercal
therapy, a number of case reports surfaced which noted
that some cysts can resolve without anti-cysticercal
therapy19. Since then, an alternative opinion has been
voiced that the acute, severe brain inflammation resulting
from their use is unnecessary because parenchymal brain
cysticercosis has a benign course and cysts will
degenerate and heal by natural evolution of the disease.
The main evidence for clinical improvement after
anticysticercal treatment is based on two independent
retrospective studies published in 199227, 28. To date there
is only one published prospective trial evaluating the
clinical evolution of patients with viable NCC treated with
anticysticercal drugs as compared with no drugs29. Overall,
there was no significant difference in the proportion free
of cysts at 6 months or 1 year, in the proportion of patients
free of seizures at the end of 2 years, or in the rates of
sequelae. Disappearance of lesions in the control group
however occurred only in cases with single lesions,
whereas nearly half of cases free of cysts in treatment arm
had multiple lesions suggesting benefit of anticysticercal
therapy for those with multiple lesions.
A recent study regarding the role of anti-parasitic
treatment to reduce the rate of seizures due to cerebral
cysticercosis found that the drug therapy reduces the
number of seizures with secondary generalisation upto
30 months of follow-up (NNT = 6)30.
Praziquantel or Albendazole?
As demonstrated by experiments in animals, praziquantel
and albendazole are both effective antiparasitic drugs
against T. solium cysticerci. The issue is: which drug is better,
for how long is it to be given, and at what dose?
Initial studies began treatment with praziquantel with low
doses like 5-10 mg/kg/day for 2 weeks, while later studies
uniformly adopted 50 mg/kg/day for 2 weeks. Some
studies even used a single dose praziquantel treatment,
and there was no difference in the rate of disappearance
of the cysts28, 29. When Albendazole became available, no
dose ranging studies were performed for it and the dose

Vol. 6, No. 2
April-June, 2005
Table III: Controversy in the management of SSCETL as neurocysticercosis38.
Argument
Pro-treatment
1. Rapid disappearance of cysts
2. Severe cases seen less frequently now.
3. Series of albendazole or praziquantel treated
patients have better resolution (fewer seizures)
than untreated patients seen at the same centres.
4. Fewer residual calcifications.
Anti-treatment
1. NCC becomes symptomatic after a period of years
as a result of onset of process of death of parasite.
2. Anti-cysticercal therapy leads to acute cerebral
inflammation, and this therapy is thus severe and
unnecessary.
3. Adverse reaction to treatment may lead to death
of the patient.
used in Hydatid cyst (15 mg/kg/day) was also used for
cysticercosis. The initial length of therapy was I month, later
reduced to 15 days and 1 week31.
Only 3 randomised controlled trials of albendazole in
SSECTL have been reported. Two studies demonstrated no
difference in radiographic resolution of lesion whereas the
third did show rapid radiographic resolution with
albendazole, but no difference in the frequency of clinical
events32-34. It was also noted that between second and third
day of therapy there was an exacerbation of the
neurological symptoms, and it was opined that anti-
parasitic therapy could be life threatening. This exacerbation
is probably due to local inflammation surrounding the
dying larvae resulting in oedema and intracranial
hypertension, and henceforth, albendazole was given
under cover of steroids.
The advantages of albendazole over praziquantel are that
the former is orally available as a once daily dose, has a
better penetration into the CSF, its concentration is not
affected when given with steroids, and it is cheaper as
compared to the latter.
Journal, Indian Academy of Clinical Medicine
Vol. 6, No. 2
Reply
1. No evidence that faster disappearance of cysts results
in better epilepsy control.
2. Less severe cases reflect improved sanitation and
fewer massive infections.
3. Inadequate control groups in initial studies.
4. No evidence that anti-cysticercal therapy results in
fewer calcifications.
1. Questionable methodology of controlled studies,
some patients persist with symptoms and live with
cysts for years.
2. Inflammation can be controlled with steroids; chronic
moderate inflammation may lead to scars similar to
or worse than those from a short, acute, severe
process.
3. Less than 10 deaths reported [mainly massive
infections] among many albendazole or praziquantel
treated cases.
Other measures
The role of surgery in the management of NCC has
significantly decreased over time and is now mainly
restricted to placement of ventricular shunts for
hydrocephalus secondary to NCC. Recently, less invasive
procedures like neuroendoscopic resection of cysts with
less morbidity than open surgery have come into
vogue35.
Corticosteroids are frequently used in the management
of NCC. The most frequent regimen is dexamethasone
at doses between 4.5 -12 mg/day36. Mannitol is
employed to treat the intracranial hypertension
secondary to NCC. Seizures secondary to NCC usually
respond well to first-line antiepileptics. Withdrawal of
antiepileptics can be achieved, but residual
calcifications on CT scan mark patients for whom the
risk of recurrent seizures is high.
Table IV shows the current proposed management
guidelines based on site and characteristics of the
lesion.

April-June, 2005 119
Table IV: Levels of evidence for the management of neurocysticercosis38.
Type Recommendation Evidence
Parenchymal cysticercosis 1. Anti-parasitic treatment alongwith steroids. II-3
Viable live cysts 2. Anti-parasitic treatment; steroids used only if side effects
related to therapy appear. II-3
3. No anti-parasitic treatment; only neuroimaging follow-up. II-3
Consensus: Anti-parasitic treatment alongwith steroids. II-3
Enhancing lesions 1. No anti-parasitic treatment; neuroimaging follow-up. I
2. Anti-parasitic treatment alongwith steroids. II-3
3. Anti-parasitic treatment; steroids only if side effects develop. II-3
Calcified cysticerci (any number) Consensus: No anti-parasitic treatment.
Extra-parenchymal cysticercosis
Ventricular Subarachnoid cysts, Consensus: anti-parasitic treatment alongwith steroids,
or Hydrocephalus ventricular shunt if hydrocephalus. II-3
Level of evidence:
I: Evidence obtained from atleast one properly randomised controlled trial.
II-1: Evidence from well-designed controlled trials without randomisation.
II-2: Evidence from well-designed cohort or case-control analytic studies, preferably from more than one research group or centre.
II-3: Evidence obtained from multiple time series with or without intervention, including dramatic results in uncontrolled experiments.
III: Opinions of respected authorities, based on clinical experience; descriptive studies and case-reports; or reports of expert committees.

References 10. Singh MK, Garg RK, Nath G, Verma DN et al. Single small
enhancing computed tomographic (CT) lesions in Indian
1. Bhargava S, Tandon PN. Intracranial tuberculomas: A CT patients with new-onset seizures. A prospective follow-up
study. Br J Radiol 1980; 53: 935-45. in 75 patients. Seizure 2001; 10 (8): 573-8.
2. Wadia RS, Makhale CN, Kelkar AN. Focal epilepsy in India
11. Sachdev HP, Shiv VK, Bhargava SK, Dubey AP et al. Reversible
with special reference to lesion showing ring or disc like
computed tomographic lesions following childhood
enhancement on contract computed tomography. J Neurol
seizures. J Trop Pediatr 1991; 37 (3): 121-6.
Neurosurg Psychiatry 1987;1298-301.
12. Singhi P, Jain V, Khandelwal N. Corticosteroids versus
3. Sethi PK, Kumar BR, Madan VS, Mohan VS. Appearing and
albendazole for treatment of single small enhancing
disappearing CT abnormalities and seizures. J Neurol
computed tomograpjhic lesions in children with
Neurosurg Psychiatry 1985; 48: 866-9.
neurocysticercosis. J Child Neurol 2004; 19 (5): 323-7.
4. Bansal BC, Dua A, Gupta R, Gupta MS. Appearing and
13. Yodnopaklow P, Mahuntussanapong A. Single small
disappearing CT abnormalities in India-an enigma. J Neurol
enhencing CT lesions in Thai patients with acute
Neurosurg Psychiatry 1989; 52: 1185-7.
symptomatic seizures: a clinico-radiological study. Trop Med
5. Chandy MJ, Rajshekhar V, Ghosh S. Single small enhancing Int Health 2000; 5 (4): 250-5.
CT lesions in Indian patients with epilepsy: clinical,
14. Varma A, Gaur KJ. The clinical spectrum of
radiological and pathological considerations. J Neurol
neurocysticercosis in the Uttaranchal region. J Assoc
Neurosurgery Psychiatry 1991; 54: 702-5.
Physicians India 2002; 50: 1398-1400.
6. Chandy MJ, Rajshekhar V, Prakash S et al. Cysticercosis
15. Rajshekhar V, Joshi DD, Doanh NQ, Van de N et al. Taenia
causing single small CT lesions in Indian patients with
Solium cysticercosis in Asia: epidemiology, impact and
seizures. Lancet 1989; 1: 390.
issues. Acta Trop 2003; 87 (1): 53-60.
7. Sawhney IMS, Thussu A, Chopra JS. Single small enhancing
16. Murthy JM, Yangala R. Acute symptomatic seizures -
CT lesions in Epilepsy. In: Chopra JS, Sawhney IMS, eds.
incidence and aetiological spectrum: a hospital-based
Neurology in Tropics. New Delhi: B.I. Churchill livingstone;
study from South India. Seizure 1999; 8 (3): 162-5.
1999; Pg. 533.
17. Sotelo J. Neurocysticercosis. Br Med J 2003; 326: 511.
8. Rajshekhar V. Aetiology and management of single small
CT lesions with seizures: understanding a controversy. Acta 18. Ahuja GK, Behari M, Goulatia RK, Jailkhani BL. Disappearing
Neurologica Scandinavica 1991; 84: 465-70. CT lesions in Epilepsy. Is tuberculosis or Cysticercosis the
9. Garg RK, Nag D. Single enhancing CT lesions in Indian cause? J Neurol Neurosurg Psy 1989; 52: 915-6.
patients with seizures: clinical and radiological evaluation 19. Mitchell WG, Crawford TO. Intraparenchymal Cerebral
and followup. J Trop Pediatr 1988; 44 (4): 204-10. Cysticercosis in Children: Diagnosis and Treatment.

120 Journal, Indian Academy of Clinical Medicine
Vol. 6, No. 2
April-June, 2005
 Pediatrics 1988; 82: 76-82.
20. Lotz J, Heuulett R, Alkert B, Bowen R. Neurocysticercosis:
Correlative Pathomorphology and MR Imaging.
Neuroradiology 1988; 30: 35-41.
21. Desai S, Bhatia K, Wadia N. Neurocysticercosis (Letter).
Neurology 1990; 40: 564-5.
22. Chacko G, Rajshekhar V, Chandy MJ, Chandi SM. The calcified
intracorporeal vacuole: an aid to the pathological diagnosis
of solitary cerebral cysticercus granulomas. J Neurol
Neurosurg Psychiatry 2000; 69 (4): 525-7.
23. Schantz PM, Sarti E, Lancarte A. Community based
Epidemiological Investigations of Cysticercosis due to Tenia
Solium: Comparison of serological screening tests and
clinical findings in two populations in Mexico. Clin Infect
Dis 1994; 18: 879.
24. Pal D, Carpio A, Sander J. Neurocysticercosis and Epilepsy
in developing countries. J Neurol Neurosurg Psychiatry 2000;
68: 137-43.
25. Tsang VC, Brand A, Boyer A. An Enzyme Linked Immuno
Electro Transfer Blot assay by Glycoprotein antigens for
diagnosing human Cysticercosis. J Infect Dis 1989; 159: 50-9.
26. Sotelo J, Guerrero V, Rubio-Donnadieu F. Neurocysticercosis:
A new classification based on active and inactive forms. A
study of 753 cases. Arch Intern Med 1985; 145: 442-5.
27. Vazquez V, Sotelo J. The course of seizures after treatment
for cerebral cysticercosis. N Eng J Med 1992; 327: 696-701.
28. Del Brutto OH, Santibanez R, Noboa CA, Aguirre R et al.
Epilepsy due to neurocysticercosis- Analysis of 203 patients.
Neurology 1992; 42: 389-92.
29. Carpio A, Santillan F, Leon P, Flores C et al. Is the Course of
Neurocysticercosis modified by treatment with
antihelminthic agents ? Arch Intern Med 1995; 155: 1982-8.
30. Garcia HH, Pretell JE, Gilman RH, Martinez SM et al. A trial of
antiparasitic treatment to reduce the rate of seizures due
to cerebral cysticercosis. N Eng J Med 2004; 350: 249-58.
31. Garcia HH, Gilman RH, Horton J et al. Albendazole therapy
for neurocysticercosis: a prospective double-blind trial
comparing 7 versus 14 days of treatment. Cysticercosis
working group in Peru. Neurology 1997; 48: 1421-7.
32. Padma MV, Behari M, Mishra NK, Ahuja GK. Albendazole in
neurocysticercosis. Natl Med J India 1995; 8: 255-8.
33. Baranwal AK, Singhi PD, Khandelwal N, Singhi SC.
Albendazole therapy in children with focal seizures and
SSECTL: A randomised, placebo controlled, double blind
trial. Pediatric Infect Dis 1998; 17: 696-700.
34. Singhi P, Ray M, Singhi S, Khandelwal N. Clinical spectrum
of 500 children with neurocysticercosis and response to
albendazole therapy. J Child Neurol 2000; 15 (4): 207-13.
35. Bergsneider M. Endoscopic removal of cysticercal cysts
within the fourth ventricle. Technical note. J Neurosurg 1999;
91 (2): 340-5.
36. Del Brutto OH, Sotelo J, Roman GC. Therapy for
neurocysticercosis: A reappraisal. Clin Infect Dis 1993; 17:
730-5.
37. Del Brutto OH, Sotelo J, White AC Jr et al. Proposed
diagnostic criteria for neurocysticercosis. Neurology 2001;
57 (2): 177-83.
38. Garcia HH, Nash TE, Takayanagui OM, WhiteAC Jr et al. Current
Consensus Guidelines for Treatment of Neurocysticercosis.
Clinical Microbiology Review 2002; 15 (4): 747-56.

BOOK REVIEW
“DOCTORS DO CRY”
Editor: Ashish Goel
Paras Publishing, Hyderabad, 1st Edition, pp 170, Rs. 150/-
‘Doctors Do Cry’ is a collection of stories written by doctors. These stories are exciting and enlightening, and provide food for
thought. It is said that without reflection we cannot see ourselves. These stories tell us of the dedication, determination, decisiveness,
and discipline of the patient on the brink of death, yet conquering the inevitable – all due to their faith in doctors and the will
power to survive and enjoy the fruits of life. Sometimes it requires contrast to appreciate the steady and the familiar. These are
stories of uncertainty of medical therapy, unfolding the misery and mystery of medicine – and above all, the situations where
doctors look within them than without. Doctors as humans are prone to some short-comings and feelings for their patients. Each
patient teaches us a lesson. Doctors may not shed tears in front of their patients or close associates but do cry in their heart on
introspection because they too are human beings caring for human beings. Patient(s) do not care about what doctors know, but
they do know that doctors care for them with concern, compassion, and courtesy. This book will bring about a positive and
prerogative change with prudence in doctor-patient relationships.
Dr. Ashish Goel is to be congratulated and complimented for his maiden effort in publishing the book with the aim to “Cure rarely,
comfort mostly, and console always”.
Dr. Anil Chaturvedi
MBBS,MD,FIAMS,FICP,FIACM,FGSI,FICS(USA),FCCP(USA),FRST,M&H(LOND)
Senior Consultant, Internal Medicine
Indraprastha Apollo Hospitals, New Delhi

Journal, Indian Academy of Clinical Medicine
Vol. 6, No. 2
April-June, 2005 121