**2. Racemose neurocysticercosis**

*among other neurotoxins causing neurovascular lesions, accompanied by increased concentration of pro-inflammatory molecules from meningeal macrophages, choroids plexus macrophages, perivascular macrophages, multinucleated giant cells, according to the number and location of the cysticercus as previously described* [33]*. At the present moment, we believe that toxins released by the T. solium cysticercus cause inflammatory changes on the perforating arteries (toxic vasculitis?) at the subarachnoid space rather than a direct effect on the cluster of parasites (mechanical compression). However, the differential of infective vasculitis should be preserved because pathological source is the presence of* 

In our series, we did not identify any case presenting immune reconstitution inflammatory syndrome, probably because we selected patients from stage I to III of AIDS not on HAART. It is interesting to know that in the brain of patients with ischaemic stroke-associated deaths, there are abundant CD3+, CD8+ and CD68+ cells in the postmortem autopsy [34]. In our study, only one patient died from Group A. We believe that low mortality rate may be related to the exclusion of patients with subarachnoid cysticercosis growing to giant size causing mass effect and obstructive hydrocephalus with mechanical compression, as already discussed [33]. The disease course in SNCC is often long in duration and cysticerci continue to grow and proliferate through tissue. This increase in volume and mechanical resistance from the brain parenchymal may cause osmotic exchange with the CSF and this one factor that may lead to a poor prognosis [35]. Obviously, selecting patients before this stage can help to investigate the effect of the SNCC on the blood vessels without an effect of associated mechanical

Evidence of carotid occlusion in cysticercosis [23, 36, 37], transient ischaemic attack of the vertebrobasilar territory [38] even in children [39] has been reported as anecdotic cases.

The most common affected vascular territory in our series was middle cerebral artery followed by posterior cerebral artery. We did not confirm any patients with SNCC and ischaemic infarct on the anterior cerebral artery territory and only one case has been reported in the

Haemorrhagic stroke (intracerebral or subarachnoid) associated with NCC and HIV was not selected in our series and some cases reported in the medical literature are not certain [41, 42]. We will investigate the association of haemorrhagic stroke and SNCC in a forthcoming research. Strengths of our study include the large sample size, geographically distinct locations of the participating clinics from the former Transkei in rural South Africa, and potential

Weaknesses of this study include the exclusion of a number of variables that may have contributed to the analysis, such as patient's response to anti-parasitic treatment and the degree of immune compromise. Better reporting of HIV status is also necessary, as over half of the patients selected were HIV-status unknown. In our study, the prevalence of SNCC without

Risk for ischaemic stroke in patients with subarachnoid NCC is almost three times more for patients with intraparenchymal NCC. Comorbidity of subarachnoid NCC in HIV-positive

*intracranial cysticercosis.*

160 Seizures

compression.

medical literature [40].

feasibility of its replication in similar regions worldwide.

hydrocephalus in patients living with NCC is 4.77%.

patients increases up to 7.6-fold.

Racemose neurocysticercosis (RC) also known as SNCC refers to a very uncommon form of NCC, with the cyst localised mainly in the subarachnoid space and basal cisterns. Usually, the scolex is absent and multiple complex small cysts may form (cluster of grapes), filling the basal cisterns, determining mass effect and distortion of adjacent structures, namely sulci, brainstem and cranial nerves [43–45], these authors consider that in racemose NCC, there is a presence of abnormally large growths of many cystic membranes without a scolex, normally without enhancement, in subarachnoid space and basal cisterns and they found on imagenology that the cysts have a thin wall without a scolex; their signal is isointense or slightly different from CSF, hypointense on T1-weighted images (T1-WIs) and fluid-attenuated inversion recovery (FLAIR), hyperintense on T2-WI, without diffusion restriction, and after contrast there is no wall enhancement. A three-dimensional balanced steady-state free precession sequence (constructive interference in steady state (CISS)), driven equilibrium (DRIVE) or contrast-enhanced MR cisternography helps to detect the underlying cysts [46]. Pamplona et al. [46] reported a case of a *43-year-old woman from Cabo Verde, with an eight-month history of right frontotemporal headaches (without releasing or aggravating factors), ataxia and loss of vision, without significant past medical history of note and no history of head trauma. Home hospital computed tomography (CT) disclosed a large intraventricular cyst, without enhancement after ionic contrast administration, distorting lateral and third ventricles, with obliterations of Monro foramina, determining non-communicating hydrocephalus, with enlargement of occipital and temporal horns of lateral ventricles and ependimary transudation.* They established that *racemose neurocysticercosis (INCC) refers to cysts in the subarachnoid space and is characterised by proliferative lobulated cysts without a scolex.* We also agree with such definition if the presence of scolex is not excluded from the definition, as discussed later. These cysts may vary in size, from 2 to 3 mm in subarachnoid space and basal cisterns, to a few centimetres when intraventricular. Intracranial hypertension and hydrocephalus are two complications that happen when there is a flow obstruction due to intraventricular cysts, arachnoiditis, ependymitis secondary to inflammatory response or mass effect in cases of very large cysts [44, 45].

It is known that in the next several months to years, there is degeneration of the cyst, with associated inflammatory response and peripheral oedema, leading to clinical symptoms and manifestations that may vary according to localisation and mass effect [43–45]. The final stage (calcified) with or without associated oedema is seen in the intraparenchymal presentation and is the main cause of epilepsy in this series; obviously, associated oedema never happens at the subarachnoid space.

The differential diagnosis depends on where the cysts are localised; if in the subarachnoid space and basal cysterns, the differential diagnoses are arachnoid cysts, neuroglial cysts, gliomas, cavernous malformations and echinococcal cysts.

Detection of cysticercal antigens by monoclonal antibody-based enzyme-linked immunosorbent assay (ELISA) in the CSF of clinically suspected patients supports the diagnosis of active SNCC.

## **3. Stroke**

Almost all clinical presentations of stroke can be seen in epileptic patients having SNCC [27, 41, 46–65]. Despite the increasing number of reports on haemorrhagic stroke to the medical literature [19, 20, 23, 24, 26, 27, 29–31, 37–41, 47–62], the prevalence of stroke secondary to NCC remains higher in IS secondary to infectious vasculitis. The most common clinical manifestations of NCC are seizure and headaches. In addition, cysticerci may cause mass effect, obstructive hydrocephalus, intracranial hypertension, cerebral infarction, vasculitis and meningitis [66, 67]. Seizures are more common in intraparenchymal NCC, resulting from cystic perilesional inflammation, new infarcts and vasculitis. Acute encephalitis-like presentation is rare, but can be the first symptom in the paediatric population [66]. Cerebrovascular complications of NCC include lacunar infarction, large-vessel disease, transient ischaemic attacks, progressive midbrain syndrome and brain haemorrhage, resulting from a multiplicity of mechanisms, including luminal narrowing due to sub-intimal cushions, vasospasm due to arteritis in midsized and small perforating vessels of the brain, and fresh thrombi [44, 45].

who *presented with relapsed subarachnoid haemorrhage possibly linked to NCC*. In addition, they performed a *literature review of all of the reported cases of aneurysmal and non-aneurysmal haemorrhagic cerebrovascular events associated with NCC until year 2011 and identified 11 such cases. The majority of the individuals were young males (mean: 38 years; 70% males). Four cases (36%) had aneurysms. Four (36%) others had negative cerebral angiograms and therefore classified as nonaneurysmal, while the remaining three (28%) did not report sufficient information to classify them. All cases with aneurysmal haemorrhage underwent successful surgical repair of the aneurysms. Seven patients received albendazole (including three who have had surgery). Three patients died; all three presented in the pre-albendazole era.* In summary, NCC should be considered in the differential diagnosis of haemorrhagic cerebrovascular events in young patients without classical

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vascular risk factors who have lived or visited NCC endemic areas [57].

*clinical evidence of cerebral ischaemia.*

all patients living in regions where NCC is endemic.

**4. Imagenology**

In 1998, using cerebral arteriography Barinagarrementeria and Cantú [27] studied 28 patients (mean age, 37 years) with subarachnoid cysticercosis admitted to their hospital from July 1993 to February 1996 and found that *15 patients had angiographic evidence of cerebral arteritis (53%); 12 of the 15 had a stroke syndrome (P = .02). Eight of the 15 patients (53%) with cerebral arteritis had evidence of cerebral infarction on MRI*. In that series, *the most commonly involved vessels were the middle cerebral artery and the posterior cerebral artery*, as we already discussed [33]. They concluded that *the frequency of cerebral arteritis in subarachnoid cysticercosis was higher than previously reported, and middle size vessel involvement is a common finding, even in those patients without* 

Some authors [58, 62] consider that NCC *is a disease with protean manifestations, which depends upon the number of parasites, their location and the degree of host inflammatory response. Most common clinical manifestations include late onset epilepsy or symptoms of intracranial hypertension and cerebrovascular complications have been reported to occur in 4–12% of patients* [58, 62]*.* In the majority of their cases, the diagnoses were ischaemic cerebrovascular events associated with vasculitis and/or thrombosis from surrounding cysts in both small- and large-diameter vessels. *Subarachnoid haemorrhages have been noted in SNCC and have been associated with cerebral aneurysms in some, but not all, cases* [58, 61]. Inflammatory aneurysms are usually located at distal intracranial arteries, not at bifurcations like congenital aneurysms, and are more commonly fusiform in shape. The wall of inflammatory aneurysms and parent vessels are extremely friable, and the possibility of intraoperative rupture is higher; in addition, inflammatory aneurysms are fusiform in shape so clipping of the aneurysm neck while preserving the parent artery is technically challenging [61]. As a result, *they are generally secured by wrapping* [59]*, clipping of the proximal artery* [64] *or trapping* [61]*.* Obviously, SNCC should be considered in the differential diagnosis of aneurysmal and non-aneurysmal haemorrhagic stroke events in

Based on our experience, imagenology is the investigation of choice for confirmation of SNCC. MRI scan is better than CT scan to identify intraventricular NCC and CT is better to confirm calcified intraparenchymal NCC, and both can be used for confirmation of SNCC but

In our region, the incidence and prevalence of ischaemic stroke due to infectious vasculitis is higher in HIV patients compared with other causes of infectious vasculitis because HIV/ AIDS is more common than other mentioned infectious diseases, at the present moment. Tuberculosis (TB) of the CNS and neurosyphilis are not uncommon problems. Unfortunately, the worse prognosis is reserved for HIV/AIDS followed by TB, neurosyphilis and others.

Stroke as a complication of NCC occurs in a very small percentage of cases, mostly involving small perforating vessels while major intracranial vessel involvement is extremely rare. Coleman et al. [47] also reported two autopsied cases of chronic cysticercal basal arachnoiditis causing large arterial territory infarcts and, in the second case, a hypothalamic mass. In their patient, *the diagnosis was established only at autopsy, which revealed SNCC causing basal arachnoiditis, major vessel vasculitis and infarcts. Histologically, case 1 showed degenerating racemose cysticercal cyst within the thick basal exudate. In the second case, remnants of the degenerated cysticercal cyst in the form of hooklets and calcareous corpuscles were identified within the giant cell inciting a granulomatous response to form a hypothalamic mass lesion mimicking tuberculoma*. These authors highlighted the importance of considering the non-tuberculous aetiologies of chronic basal arachnoiditis like SNCC before initiating therapy especially in countries endemic to both NCC and tuberculosis.

Other authors [48, 49] reported stroke *as a recognised complication of NCC, occurring in 2–12% of cases, mostly in the form of small lacunar infarcts and informed about a 51-year-old Hispanic woman, which was secondary to complete occlusion of the left internal carotid and bilateral anterior cerebral arteries. Their report represents the third reported case of internal carotid artery occlusion and the first reported case of anterior cerebral artery occlusion secondary to neurocysticercosis at that time*. Another author [50] considered that ischaemic stroke *is a relatively common but underrecognised complication of NCC and it is usually caused by inflammatory occlusion of the arteries at the base of the brain secondary to cysticercotic arachnoiditis. In most cases, the involved vessels are of small diameter and the neurological picture is limited to a lacunar syndrome secondary to a small cerebral infarct. However, large infarcts related to the occlusion of the middle cerebral artery or even the internal carotid artery have also been reported* [50]*.* Viola et al. [57] reported a patient who *presented with relapsed subarachnoid haemorrhage possibly linked to NCC*. In addition, they performed a *literature review of all of the reported cases of aneurysmal and non-aneurysmal haemorrhagic cerebrovascular events associated with NCC until year 2011 and identified 11 such cases. The majority of the individuals were young males (mean: 38 years; 70% males). Four cases (36%) had aneurysms. Four (36%) others had negative cerebral angiograms and therefore classified as nonaneurysmal, while the remaining three (28%) did not report sufficient information to classify them. All cases with aneurysmal haemorrhage underwent successful surgical repair of the aneurysms. Seven patients received albendazole (including three who have had surgery). Three patients died; all three presented in the pre-albendazole era.* In summary, NCC should be considered in the differential diagnosis of haemorrhagic cerebrovascular events in young patients without classical vascular risk factors who have lived or visited NCC endemic areas [57].

In 1998, using cerebral arteriography Barinagarrementeria and Cantú [27] studied 28 patients (mean age, 37 years) with subarachnoid cysticercosis admitted to their hospital from July 1993 to February 1996 and found that *15 patients had angiographic evidence of cerebral arteritis (53%); 12 of the 15 had a stroke syndrome (P = .02). Eight of the 15 patients (53%) with cerebral arteritis had evidence of cerebral infarction on MRI*. In that series, *the most commonly involved vessels were the middle cerebral artery and the posterior cerebral artery*, as we already discussed [33]. They concluded that *the frequency of cerebral arteritis in subarachnoid cysticercosis was higher than previously reported, and middle size vessel involvement is a common finding, even in those patients without clinical evidence of cerebral ischaemia.*

Some authors [58, 62] consider that NCC *is a disease with protean manifestations, which depends upon the number of parasites, their location and the degree of host inflammatory response. Most common clinical manifestations include late onset epilepsy or symptoms of intracranial hypertension and cerebrovascular complications have been reported to occur in 4–12% of patients* [58, 62]*.* In the majority of their cases, the diagnoses were ischaemic cerebrovascular events associated with vasculitis and/or thrombosis from surrounding cysts in both small- and large-diameter vessels. *Subarachnoid haemorrhages have been noted in SNCC and have been associated with cerebral aneurysms in some, but not all, cases* [58, 61]. Inflammatory aneurysms are usually located at distal intracranial arteries, not at bifurcations like congenital aneurysms, and are more commonly fusiform in shape. The wall of inflammatory aneurysms and parent vessels are extremely friable, and the possibility of intraoperative rupture is higher; in addition, inflammatory aneurysms are fusiform in shape so clipping of the aneurysm neck while preserving the parent artery is technically challenging [61]. As a result, *they are generally secured by wrapping* [59]*, clipping of the proximal artery* [64] *or trapping* [61]*.* Obviously, SNCC should be considered in the differential diagnosis of aneurysmal and non-aneurysmal haemorrhagic stroke events in all patients living in regions where NCC is endemic.

## **4. Imagenology**

**3. Stroke**

162 Seizures

NCC and tuberculosis.

Almost all clinical presentations of stroke can be seen in epileptic patients having SNCC [27, 41, 46–65]. Despite the increasing number of reports on haemorrhagic stroke to the medical literature [19, 20, 23, 24, 26, 27, 29–31, 37–41, 47–62], the prevalence of stroke secondary to NCC remains higher in IS secondary to infectious vasculitis. The most common clinical manifestations of NCC are seizure and headaches. In addition, cysticerci may cause mass effect, obstructive hydrocephalus, intracranial hypertension, cerebral infarction, vasculitis and meningitis [66, 67]. Seizures are more common in intraparenchymal NCC, resulting from cystic perilesional inflammation, new infarcts and vasculitis. Acute encephalitis-like presentation is rare, but can be the first symptom in the paediatric population [66]. Cerebrovascular complications of NCC include lacunar infarction, large-vessel disease, transient ischaemic attacks, progressive midbrain syndrome and brain haemorrhage, resulting from a multiplicity of mechanisms, including luminal narrowing due to sub-intimal cushions, vasospasm due to arteritis in midsized and small perforating vessels of the brain, and fresh thrombi [44, 45]. In our region, the incidence and prevalence of ischaemic stroke due to infectious vasculitis is higher in HIV patients compared with other causes of infectious vasculitis because HIV/ AIDS is more common than other mentioned infectious diseases, at the present moment. Tuberculosis (TB) of the CNS and neurosyphilis are not uncommon problems. Unfortunately, the worse prognosis is reserved for HIV/AIDS followed by TB, neurosyphilis and others.

Stroke as a complication of NCC occurs in a very small percentage of cases, mostly involving small perforating vessels while major intracranial vessel involvement is extremely rare. Coleman et al. [47] also reported two autopsied cases of chronic cysticercal basal arachnoiditis causing large arterial territory infarcts and, in the second case, a hypothalamic mass. In their patient, *the diagnosis was established only at autopsy, which revealed SNCC causing basal arachnoiditis, major vessel vasculitis and infarcts. Histologically, case 1 showed degenerating racemose cysticercal cyst within the thick basal exudate. In the second case, remnants of the degenerated cysticercal cyst in the form of hooklets and calcareous corpuscles were identified within the giant cell inciting a granulomatous response to form a hypothalamic mass lesion mimicking tuberculoma*. These authors highlighted the importance of considering the non-tuberculous aetiologies of chronic basal arachnoiditis like SNCC before initiating therapy especially in countries endemic to both

Other authors [48, 49] reported stroke *as a recognised complication of NCC, occurring in 2–12% of cases, mostly in the form of small lacunar infarcts and informed about a 51-year-old Hispanic woman, which was secondary to complete occlusion of the left internal carotid and bilateral anterior cerebral arteries. Their report represents the third reported case of internal carotid artery occlusion and the first reported case of anterior cerebral artery occlusion secondary to neurocysticercosis at that time*. Another author [50] considered that ischaemic stroke *is a relatively common but underrecognised complication of NCC and it is usually caused by inflammatory occlusion of the arteries at the base of the brain secondary to cysticercotic arachnoiditis. In most cases, the involved vessels are of small diameter and the neurological picture is limited to a lacunar syndrome secondary to a small cerebral infarct. However, large infarcts related to the occlusion of the middle cerebral artery or even the internal carotid artery have also been reported* [50]*.* Viola et al. [57] reported a patient

Based on our experience, imagenology is the investigation of choice for confirmation of SNCC. MRI scan is better than CT scan to identify intraventricular NCC and CT is better to confirm calcified intraparenchymal NCC, and both can be used for confirmation of SNCC but CT scan costs less; for establishing the stage of NCC, one of them are mandatory, and both are necessary before and after the treatment [65–69].

these locations and they found that 47 *T. solium cysts located in the basal cisterns of the subarachnoid space were diagnosed in 18 Mexican patients. A pre-treatment MRI was performed on all patients, and all four sequences (FIESTA, FLAIR, T1 SPGR, and T2) were evaluated independently by two neuroradiologists*. The mentioned authors found *FIESTA sequences allowed the visualisation of cyst membrane in 87.2% of the parasites evaluated, FLAIR in 38.3%, SPGR in 23.4% and T2 in 17.0%. Therefore, the superiority of FIESTA sequences over the other three imaging methods was statistically significant (P < 0.001). Scolices were detected by FIESTA twice as much as the other sequences did, although this difference was not significant (P > 0.05). Differences in signal intensity between CSF and parasite cysts were significant in FIESTA (P < 0.0001), SPGR (P < 0.0001) and FLAIR (P = 0.005) sequences*, and they [91] concluded that, *for the first time, the usefulness of 3D MRI sequences to diagnose T. solium cysts located in the basal cisterns of the subarachnoid space was demonstrated*. *The routine use of these sequences could favour an earlier diagnosis and greatly improve the prognosis of patients affected by this severe form of the disease.* An accurate diagnosis of this condition is important since early treatment with steroids is advised to ameliorate the subarachnoid inflammatory reaction which

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165

We thank Prof Targonska and Dr. Anwary, radiologist from Nelson Mandela Academic Hospital, and Dr. Priya Parag and her radiologist team from Inkhosi Albert Lithuli Central

Special thanks to Ms. Christine Tronson Benner, MPH Department of Biostatistics and Epidemiology College of Public Health, University of Oklahoma Health Sciences Center for

Department of Neurology, Nelson Mandela Academic Hospital, Walter Sisulu University,

[1] Foyaca-Sibat H, LdeF I-V. Clinical trial of praziquantel and prednisone in rural patients with neurocysticercosis presenting recurrent epileptic attacks. The Internet Journal of Neurology. 2002;**2**:41-50. Full article available at the URL: http://www. ispub.com/journal/the\_internet\_journal\_of\_neurology/volume\_1\_number\_2\_39/ article/clinical\_trial\_of\_praziquantel\_and\_prednisone\_in\_rural\_ patients\_with\_neu-

rocysticercosis\_presentin\_with\_recurrent\_epileptic\_attacks.html

may cause recurrent cerebral infarcts [50].

Hospital in Durban, South Africa, for their co-operation.

Humberto Foyaca-Sibat\* and Lourdes de Fátima Ibañez-Valdés \*Address all correspondence to: humbertofoyacasibat@gmail.com

her suggestions and corrections made in this report.

**Acknowledgements**

**Author details**

Mthatha, South Africa

**References**

Recently Xiao et al. [70], investigated the imaging features of NCC to provide clinicians with valuable information in the diagnosis and treatment and then investigate the imagenological features of 71 consecutive cases of NCC diagnosed by CT and MRI in 5 years time; finding parenchymal cysticerci in 53 cases (92.9%), subarachnoid cysticerci in 39 cases (68.4%), ventricular cysticerci in 13 cases (22.8%) and spinal cysticerci in 1 case; 35 cases were associated with leptomeningitis, 10 cases were with hydrocephalus and they concluded that the imaging findings of the cysticerci, including their location, numbers, cystic sizes, capsular thickness, densities and signals of the scolices, as well as the peripheral oedema, have distinct value in timely making possible diagnosis of neurocysticercosis for clinicians. Similar characteristics are found in our series [1, 7, 14–18, 33, 71–89]. Combination of SNCC and INCC in the same patient as described by Hauptman [69] was also found in our series.

Apart from CT/MRI, angiographic studies sometimes are necessary to determine the imagenological features of vascular malformations, vasculitis and occlusion of blood vessels of the brain associated with NCC. In a previous study, 15 (53%) out of 28 patients with subarachnoid cysticercosis who underwent cerebral angiography had evidence of cerebral arteritis in middle size arteries (middle cerebral artery and posterior cerebral artery) [27].

In one of the patient reported by Rocha et al. [48], MRI *demonstrated several enhancing subarachnoid cysts surrounding the occluded vessels, a right parietal racemose cyst and a left temporal large infarction area. Angiographic study showed total occlusion of left middle cerebral artery and a sub-total occlusion of right middle cerebral artery.* In the second case, CT scan *demonstrated several calcifications and a left temporal infarction area. Angiographic study showed diffuse arteritis of basilar and carotid arterial system.* In the patient reported by Levy et al. [49], the MRI demonstrated the presence of enhancing subarachnoid material surrounding these occluded cerebral arteries, providing antemortem, non-invasive documentation of the inflammatory meningeal cysticercoid reaction that was presumably responsible for the occlusive arteritis causing the cerebral infarction. In this setting, CT scan and CSF examination usually support the cause-and-effect relationship between neurocysticercosis and the cerebral infarct by showing abnormalities compatible with cysticercotic arachnoiditis. Pamplona et al. [46] *reported a case of a 43-yearold woman with an eight-month history of headaches, ataxia and loss of vision. CT and MRI showed an intraventricular cyst, causing entrapment of Monro foramina and hydrocephalus, smaller cysts at subarachnoid space in temporal lobes, Sylvian fissures, suprasellar and peri-mesencephalic cisterns, and an intra-orbital cyst. Additionally, there were acute ischaemic vascular lesions on the left thalamus and corpus callosum splenium and sub-acute ischaemic lesions of both occipital lobes.* Gilman et al. [90] reported a patient who presented with a relapsed non-aneurysmal subarachnoid haemorrhage possibly associated with subarachnoid cysticercosis and the *MRI of her brain revealed a new left subarachnoid haemorrhage involving the left suprasellar cistern, inter-peduncular cistern, left ambient cistern, and again the left Sylvian fissure. Additionally, the images showed dilatation of the lateral and third ventricles, and the aqueduct of Sylvius, with obstruction caused by cysts associated with leptomeningeal enhancement of the supracerebellar cistern.* Other authors also reported similar findings [43, 44]*.*

Without doubt, MRI is an ideal test for investigating SNCC. However, imagenological diagnosis of SNCC is usually difficult when classical MRI sequences are used [91]. Therefore, Carrillo et al. [91] evaluated the advantages of 3D MRI sequences [fast imaging employing steadystate acquisition (FIESTA) and spoiled gradient recalled echo (SPGR)] with respect to classical sequences [fluid attenuation inversion recovery (FLAIR) and T1] in visualising *T. solium* cyst in these locations and they found that 47 *T. solium cysts located in the basal cisterns of the subarachnoid space were diagnosed in 18 Mexican patients. A pre-treatment MRI was performed on all patients, and all four sequences (FIESTA, FLAIR, T1 SPGR, and T2) were evaluated independently by two neuroradiologists*. The mentioned authors found *FIESTA sequences allowed the visualisation of cyst membrane in 87.2% of the parasites evaluated, FLAIR in 38.3%, SPGR in 23.4% and T2 in 17.0%. Therefore, the superiority of FIESTA sequences over the other three imaging methods was statistically significant (P < 0.001). Scolices were detected by FIESTA twice as much as the other sequences did, although this difference was not significant (P > 0.05). Differences in signal intensity between CSF and parasite cysts were significant in FIESTA (P < 0.0001), SPGR (P < 0.0001) and FLAIR (P = 0.005) sequences*, and they [91] concluded that, *for the first time, the usefulness of 3D MRI sequences to diagnose T. solium cysts located in the basal cisterns of the subarachnoid space was demonstrated*. *The routine use of these sequences could favour an earlier diagnosis and greatly improve the prognosis of patients affected by this severe form of the disease.* An accurate diagnosis of this condition is important since early treatment with steroids is advised to ameliorate the subarachnoid inflammatory reaction which may cause recurrent cerebral infarcts [50].
