INTRODUCTION

A “seizure” is a paroxysmal alteration of neurologic function caused by the

excessive, hypersynchronous discharge of neurons in the brain. 1 The term “Epileptic

seizure” is used to distinguish a seizure caused by abnormal neuronal firing from a

nonepileptic event, such as a psychogenic seizure. 1 “Epilepsy” is the condition of

recurrent, unprovoked seizures due to abnormal, excessive neuronal activity arising

in the grey matter of the cerebral cortex.1 As per a recent study, 70 million people

have epilepsy worldwide, and with a conservative estimate of 1% as prevalence of

epilepsy, there are more than 12 million persons with epilepsy in India, which

contributes to nearly one-sixth of the global burden.2 Studies reported that the

median lifetime prevalence of epilepsy was 7.06 per 1,000 persons with an annual

incidence of 67.77 per 100,000 persons.3 It is age-dependent and higher in children

and elderly persons than in young adults.

Although most of the patients who have epilepsy will have good control of this

disease with the use of antiepileptic drugs, up to 20% of patients continue to have

seizures despite the best medical treatment.4 Therefore finding out the etiology will

give a significant edge to the patients in terms of treatment and control of seizures.

Many neuroradiological investigations can be utilized to diagnose and find out

the etiology of the lesion which include x-ray of skull, pneumocephalography, carotid

angiography, CT and MRI. MRI has the capacity for multiplanar imaging, has an

excellent soft tissue contrast, allowing for detailed depiction of anatomy, and is free

of beam – hardening artifact in basal brain that occurs with CT. MRI gives the

precise location and histological nature of lesions, which is of immense help to both

clinicians as well as neurosurgeons in deciding an accurate method of treatment.

1
Coregistration of MRI with functional imaging modalities like SPECT and PET has

also been proven to be of great value in localizing the structural and functional

alteration.

Patients presenting with seizures can often turn out to be a clinical challenge

to physicians. When compared to any other diagnostic modality, MRI gives the most

precious information to the physician and is an appropriate neuroimaging study of

choice in patients with seizures/epilepsy. MRI is proven to be the most meaningful

procedure in the diagnosis, treatment and follow-up of patients with inflammatory/

infectious lesions of the brain like tuberculoma, cysticercosis, encephalitis and

brain abscess. MRI also has a role in epilepsy surgery as well, in identifying the

epileptogenic focus, depicting the topographic relationships between epileptogenic

lesion and the eloquent regions of brain. Post-operative MRI can detect reasons for

failure of surgery such as inadequate resection and can also monitor tumor

recurrence on follow up imaging. MRI is especially useful for the prognostication of

post-operative seizure control.

The current study has been undertaken to check the utility of MRI in seizures/

epilepsy by studying various MRI findings in patients presenting with various types of

seizures.

2
 AIMS & OBJECTIVES

1. To study the spectrum of MRI findings in patients with seizures.

2. To evaluate MRI positivity in various types of seizures.

3
 REVIEW OF LITERATURE

Medical imaging has witnessed significant changes in both

technologica l and clinical arenas since the discovery of x-rays in

1895 by Wilhelm Conrad Roentgen – a German physicist. After that, C-J

Gorter, a Dutch physicist, proposed Nuclear Magnetic Resonance (NMR) in

1936, which formed the basis for modern Magnetic Resonance Imaging

(MRI). It was followed by Theory of spin echoes by Hahn (1950), the

concept of Fourier transformation of NMR signal by Ernst and Anderson i

(1966), selective slice excitation by Peter Mansfield (1974) and whole-body

MRI using field focusing by Raymond Damadian (1978). In MRI, three

gradient coils are used, each with a separate power supply and each under

independent computer control. They permit slice selection and code position

dependent information into the NMR signal. Radio Frequency (RF) coils are

used to transmit radio waves at near Larmor frequency and signal is

received, which is then processed and converted to digital images.5 MRI is

now one of the most commonly used imaging modalities with great

accuracy to diagnose various pathological lesions.

BRIEF REVIEW OF BRAIN ANATOMY AND EMBRYOLOGY

An understanding of brain development and sectional anatomy

is vital for interpretation of neuro-radiological studies.

Brain Development:

At the beginning of the 3rd week, the central nervous system

4
(CNS) appears as a plate of thickened ectoderm, the neural plate. It is

located in the middorsal region in front of the primitive pit. Its lateral

edges soon become elevated to form the neural folds. The neural

folds elevate further, approach each other in the midline, and finally

fuse, thus forming the neural tube.6

By the 4th week of gestation, three vesicular dilations a r e w

formed at the rostral portion of the neural tube, defining the

forebrain (prosencephalon), midbrain (mesencephalon), & hindbrain

(rhombencephalon).

By the 5th week of gestation, the developing forebrain is divided into a

cephalic telencephalon and a caudal diencephalon. The developing

hindbrain is subdivided into a cephalic portion called metencephalon and a

caudal portion called myelencephalon. The metencephalon later forms

the pons and cerebellum while the myelencephalon forms the medulla

oblongata.7

Fig. 1: Brain vesicles and the adult derivatives

Telencephalic end of the neural tube gives bilateral diverticula

which form the cerebral hemispheres. The hemispheres undergo complex

5
expansion and folding with formation of permanent primitive fissures by

the 4th month. The developing brain is divided into the cerebrum,

cerebellum and spinal cord by three major flexures, which are called the

midbrain, pontine and cervical flexures. Early in development the cerebral

hemispheres are smooth-surfaced (lissencephalic), and a germinal matrix of

primitive cells surrounds each lateral ventricle. Cells from the germinal

matrix proliferate, migrate outward to the cortex in an "inside out"

sequence, and mature as neural and glial cells. The germinal matrix is

forme d at about 7 weeks gestational age and i t involutes at about

28 to 30 weeks, although it persists a s focal cell clusters up to weeks

36 through 39.8 During the sixth and seventh fetal months, the cerebral

surfaces convolute to form primitive gyri and sulci. Thus, the adult pattern

can already be recognized towards the end of gestation. Concomitant with

cortical development is the formation of fiber tracts, including the

commissures between the two cerebral hemispheres.

Gross Anatomy:

The brain lies in the cranial cavity and it is continuous with the spinal

cord through the foramen magnum. It is covered by three layers of

meninges, namely dura matter, arachnoid and piamater from outside to

inside. The brain is grossly divided into three major parts, which, in

ascending order from the spinal cord are, the hindbrain, the midbrain,

and the forebrain.

Hindbrain: subdivided into the medulla oblongata, the pons, and the cerebellum.

6
1. Medulla Oblongata: conical in shape. connects pons (superiorly) to

the spinal cord (inferiorly). It contains many nuclei and serves as a

conduit for ascending and descending nerve fibers.

2. Pons: Situated anterior to the cerebellum, inferior to the midbrain and

superior to the medulla oblongata. It also contains many nuclei,

ascending and descending nerve fibers.

3. Cerebellum: It is Situated posterior to the pons and the medulla

oblongata in the posterior cranial fossa. It consists of two hemispheres

which are connected by vermis. The cerebellum is connected to the

brainstem structures by the cerebellar peduncles. Super i o r , middle

and inferior cerebellar peduncles connect cerebellum with

midbrain,pons and medulla by the inferior cerebellar peduncles

respectively. The surface layer of each hemisphere is called the cortex

and is composed of gray matter. The cortex is thrown into folds, or

folia, separated by closely set transverse fissures. Certain masses of

gray matter are embedded in white matter, the largest of these is

known as the dentate nucleus.9

Midbrain: It is the narrow part of the brain that connects the forebrain to

the hindbrain. It contains many nuclei and bundles of ascending and

descending nerve fibers.

Forebrain: further divided into diencephalon and cerebrum.

Diencephalon: It is completely hidden from the surface of the brain.

It consists of dorsal thalamus and a ventral hypothalamus. The thalamus

is a large egg-shaped mass of gray matter which lies on either side of the

7
third ventricle. The hypothalamus forms the lower part of the lateral

wall and floor of the third ventricle.9

Cerebrum: The largest part of the brain and consists of two cerebral

hemispheres, which are connected by a big mass of white matter called

the corpus callosum. The hemispheres are separated by a cleft, the

longitudinal fissure, into which, the falx cerebri projects. The surface

layer of hemispheres is ca lle d the cortex, a n d is composed of gray

matter. The cerebral cortex is thrown into folds called gyri, separated by

fissures called sulci. Large sulci are used to subdivide the surface of each

hemisphere into lobes. The lobes are named after the bones of the cranium

under which they lie. Within the hemisphere, there is a central core of white

matter and several large masses of gray matter called the basal ganglia.

Corona radiata, a fan-shaped collection of nerve fibers, passes in the white

matter to and from the cerebral cortex to the brainstem. The corona radiata

converges on the basal ganglia and passes between them as the internal

capsule. The basal ganglia consists of a tailed nucleus medial to the internal

capsule which is called the 'caudate nucleus' and a lens-shaped nucleus

lateral to the internal capsule, which is called 'the lentiform nucleus', and in

turn consists of 'putamen' and 'globus pallidus'9

8
Fig.3 : A & B: Lateral and Medial views of the cerebral hemisphere showing

various lobes

Ventricular System:

Ventricles are the cavities within the brain t h a t contain the

cerebrospinal fluid (CSF). There are two lateral, one third and one fourth

ventricles. The two lateral ventricles are present in cerebral hemispheres

and communicate through the foramina of Monro with the third ventricle.

The third ventricle is a slit like cleft present between the two thalami. It

communicates with the fourth ventricle through the cerebral aqueduct of

Sylvius. The fourth ventricle is present posterior to the pons and medulla

and anterior to the cerebellum. It communicates with the subarachnoid

space through three foramina in its roof and continues distally with the

central canal of the spinal cord.9

CSF is secreted by specialized structure called 'Choroid plexus' or

'plica choroidea' located in the ventricular lining. CSF flows through the

ventricles and subarachnoid spaces, and supports the central nervous

system. CSF is absorbed primarily through the arachnoid villi into the

superior sagittal sinus.9

9
 BLOOD SUPPLY OF THE BRAIN:

1. Arterial syst e m of the Brain: The brain is supplied by the two

internal carotid and two vertebral arteries. All these arteries and

their branches anastomose on the inferior surface of the brain to

form the circle of Willis.

a. Internal Carotid arteries: The intracranial part of the internal carotid

arteries divides into anterior and middle cerebral arteries. The anterior

cerebral artery (ACA) supplies the medial surface of the cerebral

hemisphere from the frontal pole to the parieto-occipital sulcus. The

penetrating branches of the ACA supply blood to the anterior portion

of the putamen and caudate nucleus and the anteroinferior part of

the internal capsule. The middle cerebral artery (MCA) supplies the

lateral convexity of the cerebral hemisphere. The penetrating branches

of MCA supply the internal capsule, caudate nucleus, putamen and

globus pallidus.9

b. The vertebrobasilar arteries: The two vertebral arteries join to form

the basilar artery. The basilar artery divides into two posterior

cerebral arteries (PCA). The PCA supply the midbrain, thalamus,

lateral and medial geniculate bodies, occipital lobe and inferior

surface of the temporal lobe.

The other branches of the vertebrobasilar arteries supply pons,

medulla, cerebellum, and anterior part of the spinal cord.9

2. Venous anatomy of the Brain:

The venous system of the brain constitutes dural venous sinuses and
10
cerebral veins. The cerebral veins in turn are divided into two groups:

superficial (cortical) and deep veins. Superficial or cortical veins mainly

drain in the lateral surface of the cerebral hemispheres into the

cavernous and superior sagittal sinuses. Deep cerebral veins include

medullary veins, subependymal veins, the basal veins and the vein of

Galen. They mainly drain the deeper layers of cerebral hemisphere into

the straight sinus.9

Fig. 4: Cortical territories of the three cerebral arteries

Fig.5: Venous anatomy of brain

11
REVIEW OF ESSENTIAL CLINICAL CONCEPTS

Seizure10 is “a transient occurrence of signs and/or symptoms due to an abnormal

excessive or synchronous neuronal activity in the brain”

ILAE operational clinical definition of epilepsy10 is “at least two unprovoked seizures

occurring more than 24hours apart.”

An epileptic seizure is a clinical manifestation of abnormal, excessive neuronal

activity arising in the grey matter of the cerebral cortex due to a neurological insult.

The disorganized neuronal activity can be a purely electrophysiological event

resulting in no clinically evident seizure or it can manifest as a seizure that is related

to a specific site of the abnormal activity.

CLASSIFICATION:

The most widely used classification of epileptic seizure is ILAE principally based on

clinical seizure type and interictal EEG findings.

INTERNATIONAL LEAGUE AGAINST EPILEPSY CLASSIFICATION OF

EPILEPTIC SEIZURES (1981)11

Partial seizures

Simple partial seizures (consciousness not impaired)

 With motor signs (including Jacksonian versive and postural)

 With somatosensory or special sensory symptoms

 With autonomic symptoms

 With psychic symptoms

12
  With mixed symptoms

Complex partial seizures (consciousness impaired)

 Simple partial-onset followed by impaired consciousness.

 With impaired consciousness at onset

 With automatisms.

Partial seizures with secondarily generalization

Generalized seizures of non- focal origin (convulsive or non- convulsive)

Absence seizures

 Typical absence

 Atypical absence

Myoclonic seizures

Clonic

Tonic seizures

Tonic-clonic seizures

Atonic seizures

Unclassified epileptic seizures

New classification:12

13
 Classification of epilepsy syndromes has also been done based on

factors such as, age of the patient, associated neurological abnormalities,

seizure type. It may be helpful in predicting the prognosis and directing

towards a specific therapy.

Modified ILAE classification of epileptic syndromes (1989)13

I. Idiopathic epilepsy syndrome (focal or generalized)

a. Benign neonatal convulsions (familial or non- familial)

b. Benign childhood epilepsy

i. With central mid temporal spikes

ii. With occipital spikes

c. Childhood / Juvenile absence epilepsy.

d. Juvenile myoclonic epilepsy.

e. Idiopathic epilepsy otherwise unspecified

14
 II. Symptomatic epilepsy syndromes (focal or generalized)

a. West syndrome (infantile spasm)

b. Lennox Gestaut syndrome

c. Early myoclonic encephalopathy

d. Epilpesia partialis continua

i. Rasmussen syndrome (encephalitic form)

ii. Restricted form

e. Acquired epileptic aphasia (Landau Kleffner syndrome)

f. Temporal lobe epilepsy

g. Frontal lobe epilepsy

h. Posttraumatic epilepsy

i. Other symptomatic epilepsy not specified.

III. Other Epileptic syndromes of uncertain or mixed classification.

a. Neonatal seizures

b. Febrile seizures

c. Reflex epilepsy

d. Other unspecified

Causes of Seizures:14

Seizure/ epilepsy occur as a result of dynamic interplay between

endogenous factors, epileptogenic factors and precipitating factors. Precipitants

include those due to intrinsic psychological or physical stress, sleep deprivation or

hormonal changes associated with the menstrual cycle, exogenous factors such as

exposure to toxic substances and certain medications. A seizure disorder can be

caused by local factors such as tumors, infections, inflammation etc. There are

15
genetic factors that result in structural changes that can cause epilepsy, and there

are numerous acquired causes of epilepsy which include broad groups of

abnormality such as vascular, neoplastic, degenerative, traumatic, post-infective and

metabolic causes.

Common causes of seizures based on age:14

Neonates (< 1 month) Perinatal hypoxia and ischemia

Intracranial hemorrhage and trauma

CNS infections

Metabolic disturbances

Drug withdrawal

Developmental disorders

Genetic disorders

Infants and children Febrile seizures

(> 1 month to < 12 years) Genetic disorders

CNS infections

Developmental disorders

Trauma

Idiopathic

Adolescents (12-18 years) Trauma

Genetic disorders Infection

Brain tumors

Illicit drug use

Young adults (18-35years): Trauma

Alcohol withdrawal

16
 Illicit drug use

Brain tumors

Idiopathic

Older adults (> 35 years): Cerebrovascular disease

Brain tumor

Alcohol withdrawal

Metabolic disorders

Alzheimer and degenerative diseases

REVIEW OF MRI RELATED LITERATURE IN EVALUATION OF SEIZURES

MRI has revolutionized neuroimaging and is the best method of

noninvasive structural evaluation of the brain. The MRI findings in patients with

seizure disorders may be extremely variable. The variation can range from a normal

scan to a lesion indicated by altered signal intensity in different sequences. MRI is

usually performed to define the pathological processes, be it structural or owing to

changes in the local chemical environment, such as edema or gliosis.

A large amount of work has been done on the role of MRI in the evaluation of

patients with seizures or epilepsy.

Amritpal Singh Multani et al15 studied 250 patients (138 males and 112 females)

with focal seizures presenting in OPD or IPD with exclusion of idiopathic generalized

epilepsy, acute head trauma, febrile seizures, and acute infarct/hemorrhage cases.

The study was conducted using 1.5 Tesla MRI with various protocols. MRI showed

normal study in 108 cases (43.2%), 58 cases (23.2%) of neuroinfection, 39 cases

(15.6%) of gliosis, 25 cases (10%) of neoplasms, 15 cases (6%) of developmental

anomalies, two cases (0.8%) of Rasmussen encephalitis and hypoxic-ischemic

17
encephalopathy and one case (0.4%) of vascular anomaly. The study concluded that

CNS granulomatous pathology (predominantly NCC) and gliosis/ encephalomalacia

were the two most common abnormalities detected on MRI. The majority of

structural epileptogenic abnormalities are detected by MRI, making it a superior

neuroimaging modality with no radiation exposure and higher sensitivity but subtle

abnormalities are missed giving false negative results; therefore employing

appropriate imaging protocols and performing dedicated pulse sequences is

essential.

Dr. Kumar Ashok Charan et al16 studied 72 patients with seizure disorder who

underwent MRI in Department Of Radiology, Bokaro General Hospital, Bokaro,

Jharkhand and the MR examination revealed pathological findings in 31 out of 72

patients. They include Stroke (22.5%), mesial temporal sclerosis (22.5%),

tumors/vascular abnormalities (19.3%), Infections (16.1%), Developmental disorders

(12.9%), and Phacomatosis (6.4%). The study concluded that MRI play a significant

role in patients presenting with seizures and helps to identify the cause of the

seizures.

Feldman RE et al17 studied 37 patients with focal epilepsy (based on clinical and

electroencephalogram (EEG) data, with non-lesional MRIs at clinical field strengths)

and 21 healthy controls in the 7T imaging study. 25 patients had findings with

epileptogenic potential. In 5 patients these were definitely related to their epilepsy,

confirmed through surgical intervention. In 3 patients, they co-localized to the

suspected seizure onset zone and likely caused the seizures. 10 patients had

cortical lesions with epileptogenic potential that did not localize to the suspected

seizure onset zone. In 7 patients, the imaging findings co-localized to the suspected

seizure onset zone but were not the definitive cause. Multiple other findings of

18
uncertain significance were found in both epilepsy patients and healthy controls. The

SWI sequence was instrumental in guiding more targeted inspection.

E Rahimian et al18 studied 198 (100 female and 98 male) patients with focal seizure

who were referred to one of the imaging centers. The range of age was between 1-

71 years. The study was obtained on a 1.5 Tesla MRI scanner and a three

dimensional T1 -weighted SPGR sequence was first acquired with slice thickness of

1.5mm and then FLAIR T2- weighted images were obtained with the slice thickness

of 4mm. MRI data were transferred to PACS workstation for analysis and diagnosis .

127 cases (64%) had normal MRI, 21 cases (10.5 %) temporal sclerosis,15 cases

(8%) ischemia, 14 cases (7%) tumor, 8 cases (4%) gliosis, 8 cases (4%)

developmental anomaly 4 cases (2% ) focal atrophy and 1 case (0.5%) vascular

anomaly. The study concluded that although a routine MRI would exclude ominous

structural substrates that require urgent treatment, subtle structural substrates such

as hippocampal sclerosis, which present as intractable seizure will be missed.

Performing dedicated MRI pulse sequences and optimization of imaging parameters

are essentials to detect such subtle substrates.

Arti Anand et al19 studied 95 children under the age of 12 years over a period of 2

years who presented with epilepsy. Patients with trauma and febrile seizure

disorders were excluded. Conventional and contrast MRI was performed in all cases

and lesions were characterized in location, signal intensity, and other features. The

mean age group of the study population was 4 years 3 months. Generalized seizures

constituted the major seizure group being present in 66.3%. Results showed

infection (29.8%) as the most common etiology followed by anoxia and hypoxic-

ischemic encephalopathy. Mesial temporal sclerosis (57.1%) was the most common

pathology seen in isolated temporal lobe epilepsy. Demyelinating diseases and

19
neoplasm constituted 3.6% patients each. The study concluded that MRI is the

imaging modality of choice in the evaluation of pediatric patients presenting with

epilepsy. Proper MRI seizure protocol helps to establish the correct diagnosis, plan

the management according to diagnosis as well as helps in prognosis

Gulati et al20 studied 170 children with chronic epilepsy and MRI revealed 64

tuberculomas, 27 cases of cysticercosis and 3 gliomas. It was concluded that MRI

was proven to be an excellent modality in demonstrating and characterising the

intracranial lesion.

IJ Craven et al21 reviewed from 2000 adult patients on MRI with localization related

epilepsy in 2005 to 2011 using a standard epilepsy protocol. The study revealed

61% normal, 36% abnormal and 2% non-diagnostic. In abnormal patients 53% MTS,

18.3% cortical malformations, 10.9% gliosis and infarcts, 7.1% vascular

malformations and 5.1% tumours.

Ponnatapura J et al.,22 in a prospective study conducted over an 18-month period,

studied 129 patients who presented with new-onset seizures with both MRI and

EEG. MRI detected potentially epileptogenic lesions in 59 patients (47%) and the

frequency of epileptogenic lesions was highest in patients who had focal-onset

seizures (81%). The most common lesion type was infection and inflammation

(28%), with neurocysticercosis being the most common, followed by mesial temporal

sclerosis, ischemia, and tumor. About 37% of epileptogenic lesions were missed by

standard protocol, but they were detected on a dedicated seizure protocol MRI. The

diagnostic yield of EEG was 31%. Abnormal MRI and EEG were concordant in 18%

of patients, with EEG being normal in 37% of patients with epileptogenic lesions.

Von Oertzen et al.23 studied 123 patients of intractable epilepsy as a part of

presurgical evaluation MRI and concluded that sensitivity of "non-expert" reports of

20
standard MRI reports for focal lesions was 39%, of "expert" reports of standard MRI

50%, and of epilepsy dedicated MRI 91%. Dedicated MRI showed focal lesions in

85% of patients with "non-lesional" standard MRI. The technical quality of standard

MRI improved during the study period, but "non-expert" reporting did not. In

particular, hippocampal sclerosis was missed in 86% of cases. Neuropathological

diagnoses (n=90) were predicted correctly in 22% of "non-expert" standard MRI

reports but by 89% of dedicated MRI reports.

P Conlon et al.24 in their case control study, studied 50 patients with epilepsy and

14 healthy controls using both MRI and CT. major pathologies were identified with

MRI supplemented by CT. Analysis of spin-lattice (T1) relaxation times was done

and significant differences between cases and controls were observed, especially in

the temporal lobes. Patients with generalized seizures showed increased T1 values

in the thalamus and patients with focal seizures showed prolonged T1 values on the

ipsilateral side. They conclude that MRI can effectively localize epileptogenic areas.

Hakami et al.25 studied 993 patients with epilepsy, out of which 764 patients

underwent MRI brain and potentially epileptogenic lesions were detected in 177

(23%). The frequency of potentially epileptogenic lesions was higher in patients who

were diagnosed as having an epileptic seizure (28%) than in those with a non-

epileptic event (8%) (p < 0.001), and highest in those who had focal-onset seizures

(53%) (p < 0.001). The most common lesion type in patients with focal seizures was

gliosis or encephalomalacia (49%). Other common lesion types were tumors (15%),

cavernomas (9%), and mesial temporal sclerosis (9%). Abnormal MRI and EEG

were concordant in 18% of patients, with EEG being normal in 55% of patients with

epileptogenic lesions.

Rajashekhar Muchchandi, Nandini Takalaki26 studied 60 patients with seizures in

21
a tertiary care hospital, Karnataka, using MRI and the examination revealed

pathological findings in 30 out of 60 patients (50%) which included, cerebral infarct

with gliosis (20%), NCC (6.66%), atrophy (6.66%), gliomas (1.66%), cortical

malformations (3.34%),tuberculoma (3.34%), venous thrombosis (3.34%),

cavernoma (3.34%), meningioma (1.66%).

Gaurav Kaushik et al.27 studied 150 cases of epilepsy and MRI was normal in

48.7% cases while it showed abnormalities in the rest. The abnormalities include

Infarct with gliosis (24.7%), neurocysticercosis (6.7%), cerebral atrophy (5.3%),

tuberculoma (3.3%), venous thrombosis (2.7%), developmental malformations

(2.7%), glioma (1.3%), cavernoma (1.3%), tuberous sclerosis (1.3%), meningioma

(0.7%), cerebral abscess (0.7%) and Sturge Weber syndrome (0.7%). They

concluded that MRI should be the first investigation of choice in epileptic syndrome,

cerebrovascular disease with seizures, vascular malformations and developmental

cortical malformations.

Bronen RA et al.28 studied 117 patients (56 females, 61 males) with medically

refractory epilepsy using both CT and MRI. When compared to the post-surgical

histopathological findings, MRI had a sensitivity of 95% and specificity of 87% while

CT had a sensitivity of 32% and a specificity of 93%. It was concluded that MRI is

way more superior to CT and that CT has no role in the diagnostic evaluation of

medically refractory epilepsy.

Gyimesi C. et al.29 studied 42 patients underwent presurgical evaluation including

EEG and MRI showed amygdaloid lesions without hippocampal abnormalities. Of 33

patients with infrequent spikes, 79% became seizure free, while 9 patients with

frequent spikes, only 4 had favorable surgical outcome.

22
BRIEF REVIEW OF CLINICAL ASPECTS AND MRI FEATURES OF VARIOUS

LESIONS THAT CAN CAUSE SEIZURES:

CNS INFECTIONS:

1) NEUROCYSTICERCOSIS:30

Neurocysticercosis (NCC) is an infection caused by the larval stage of Taenia solium

(pork tapeworm). Humans become infected by ingesting the eggs from contaminated

water or uncooked food. The eggs hatch and release the larvae which disseminate

via the bloodstream and enter the brain. NCC can be parenchymal (involving brain

parenchyma) and/or extra parenchymal (subarachnoid spaces, ventricles). Seizures

are usually caused by the parenchymal form of NCC. Most parenchymal NCC cysts

are small (a few mm to 1cm) and seizures usually occur as a result of inflammatory

response to the dying and degenerating parasite. Clinical and MRI findings depend

on number, size, location, viability and stage of cyst degeneration.

MR imaging features:30

MRI findings depend on several factors like number and location of parasites, stage

of evolution of the larval lesions, host inflammatory response, associated

complications like hydrocephalus and vascular disease. A single patient can present

lesions in different stages simultaneously. There are 4 recognized stages.

Vesicular (quiescent) stage: The cysticercus larva is viable and elicits few

inflammatory changes in the surrounding tissues. The cyst has a thin wall and the

cyst fluid has SI similar to CSF in all sequences. In viable cysts, an eccentrically

located mural nodule may be seen representing the scolex. FLAIR image shows the

23
scolex as an eccentrically punctuate bright signal intensity within the cysts. FLAIR

images detect a significantly higher number of scolices than other sequences which

is helpful in diagnosis of NCC. Lesions are not associated with perilesional edema

and contrast enhancement is typically absent. As per the revised diagnostic criteria

for NCC, cystic lesions showing the scolex is an absolute criteria for diagnosis.

Colloidal vesicular stage: As inflammatory reaction develops around the

cysticercus, its wall thickens and the vesicular fluid becomes gelatinous with colloidal

content. Cystic fluid is slightly distinct from that of CSF in all sequences; it is

hyperintense to CSF on T1WI. Perilesional edema is striking. Contrast enhancement

of cyst wall gives ring enhancement appearance. The scolex begins to show signs of

degeneration with a gradual decrease in the size of the lesion.

Granular nodular (healing) stage: The parasite is dead and its wall is retracted.

The lesion begins to mineralize and becomes semisolid as it is progressively

replaced by granulomatous tissue. There is substantial decrease in the perilesional

edema and nodular or faint ring enhancement is seen on contrast administration.

Nodular calcified (inactive) stage: The lesion is entirely mineralized. These lesions

appear as small hypointense nodules on both T1WI and T2WI and will bloom on

SWI/ T2*GRE images. These lesions won‟t enhance usually. CT study will detect

these lesions better. Some lesions may show persistent contrast enhancement on

MRI and may lead to active inflammation during therapy.

MRS usually shows decreased NAA peak and increased lactate, succinate,

acetate, alanine levels.

24
 Extraparenchymal NCC can be seen involving ventricles, especially fourth

ventricle. The SI of the cyst is slightly different from CSF. Hydrocephalus is

commonly seen due to obstruction of CSF flow. The lesions wont usually enhance.

Subarachnoid NCC usually involves sylvian fissures and basal cisterns. The cysts

are isointense to CSF and usually do not enhance. There is associated mass effect

and cause local subarachnoid enlargement. The scolex is rarely seen.

Large, multilobulated, grape like NCC lesions can be seen involving basal

cisterns, without any obvious scolex. This variety of NCC is called “racemose NCC.”

L.T. Lucoto, et al30 collected MR images of 115 patients over a period of 3 years

and studied the potential of MRI for detection of NCC lesions, especially scolex.

They concluded that FLAIR images were more sensitive in detecting the scolex,

while highest number of lesions were identified with gadolinium-enhanced T1C+

series (coronal or sagittal).

Sanchetee et al,31 studied 150 NCC cases collected over a period of 17 years and

found that 127 out of 150 had epilepsy. Generalized seizures were more common

followed by simple and complex partial seizures. MRI was done in 8 cases and was

found to be more sensitive in demonstrating various stages of non-calcified

cysticercosis.

2) CNS TUBERCULOSIS:

Tubreculosis is a granulomatous infection characterized by caseous central necrosis.

Tuberculosis of CNS comprises 10% of all TB cases and 20% of TB cases in

immuno-compromised patients.32 Tuberculous meningitis and tuberculoma are the

two most important manifestations of tuberculosis of the central nervous system.

Leptomeningeal tuberculosis can cause hydrocephalus, neuropathies, and deep

25
gray matter infarction, while parenchymal tuberculomas can be single or multiple and

can result in seizures. It‟s a common occurrence that both leptomeningeal and

parenchymal TB are found in many patients.

MRI findings are usually nonspecific and depend on the amount of inflammatory

cells, gliosis, and free radical deposition in the granuloma as a result of host‟s

hypersensitivity reaction to the bacillus.

MRI Features:33

Leptomeningeal TB shows nodular leptomeningeal enhancement on contrast MRI,

while MRI features of the individual tuberculomas depend on whether the granuloma

is non-caseating, or caseating with a solid center, or caseating with a liquid center, or

calcified.

Lesion T1WI T2WI FLAIR DWI T1 C+

Non Iso- to Hyperintense No No Homogeneou

caseating hypointense suppressio restrictio s

granuloma n n enhancement

Caseating Iso- to Hypointense No No Homogeneou

granuloma hypointense suppressio restrictio s or ring

with n n enhancement

hyperintens

e rim

Caseating Iso- to Hypointense Partial May or Ring

granuloma hypointense rim with suppressio may not enhancement

with with central n show

26
central hyperintens hyperintensit restrictio

liquefactio e rim y n

Calcified Iso- to Hypointense No No No

granuloma hypointense suppressio restrictio enhancement

n n

MR spectroscopy plays a significant role in differentiating tuberculomas from other

ring enhancing lesions. A prominent lipid peak at 1.3 ppm is characteristic MRS

feature of tuberculomas. Recent studies showed that the presence of

guanidinoacetate peak at 3.8 ppm is characteristic of tuberculomas. Tuberculomas

with heterogeneous SI on T1WI and T2WI with heterogeneous post-contrast

enhancement may show a choline peak at 3.32 ppm in addition to the lipid peak at

1.3 ppm, probably because of high cellularity in this variety of tuberculoma.

P.Salgado, et al.34 studied 6 patients with intracranial tuberculoma with MRI and the

signal properties of the tuberculoma on the T2-weighted sequences varied according

to the stage of evolution of the lesion. All the lesions showed prolongation of T1

relaxation time. Mature tuberculomas had a dark necrotic center surrounded by an

isointense capsule which was, in turn, is surrounded by edema. The center of the

lesion was hyperintense in one patient, probably because of liquefaction and pus

formation.

R. James Salway, et al35 reported a case of an HIV patient presenting with new-

onset seizure, whose MRI showed leptomeningeal enhancement with multiple

tuberculomas in the left occipital parasagittal region and the patient recovered well

27
on administration of anti-tubercular drugs.

Naser UAMA, et al.36 studied 925 intracranial space occupying lesions with seizures

and found 1.4% intracranial tuberculoma and followed after treatment, 66.6%

responded well to medical treatment and 33% failed to respond. Remarkable

improvement of intracranial lesions within 6 weeks and complete resolution of the

lesions within 12 weeks was found.

CEREBRAL INFARCTION:37

Cerebrovascular disease is one of the common causes of epilepsy and stroke is the

common cause of seizures in the elderly population. Studies suggest that around

11.5% of patients with stroke are at risk of developing post‐stroke seizures within five

years. Early onset seizure is the one which occurs within 2 weeks of stroke and

delayed/ late onset seizure is the one which occurs after 2 weeks. Nearly 45% of

early onset post‐stroke seizures occur within the first 24 hours while late onset

seizure has a peak within 6 to 12 months after the stroke. LAte onset seizures also

have a higher recurrence rate of up to 90%. Epilepsy develops in nearly one third of

early onset and half of late onset seizures.

Stroke is grossly classified as ischemic and hemorrhagic. The mechanisms

postulated for seizures in ischemic stroke are increase in intracellular Ca2+ and Na+

with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia,

metabolic dysfunction, global hypoperfusion, and hyperperfusion injury (particularly

after carotid end arterectomy). Seizures after haemorrhagic strokes are usually due

to irritation by various products of blood metabolism. Late onset seizures can be

associated with persistent changes in neuronal excitability and gliotic scarring.

28
 In ischaemic strokes, severity of the initial neurological deficit, severity of

persistent disability after the stroke, larger lesion, involvement of multiple sites,

cortical damage, and hippocampal involvement are factors that predict the likelihood

of developing post stroke seizures. Embolic stroke is considered as a risk factor for

early post stroke seizures.

Post‐stroke seizures typically follow a localization related (focal) seizure

semiology with upto two third cases presenting with partial seizures and the

remaining one third of cases may present with tonic‐clonic (generalised) seizures.

Early onset seizures usually present with a focal onset while generalised tonic‐clonic

seizures are more common with late onset seizures.

MRI features of infarction:5

Acute infarction is characterized by T1 hypo and T2/FLAIR high intensity area in

the specific arterial distribution. The increase in vasogenic edema results in gyral

swelling and sulcal effacement. Absence of arterial flow void can be detected.

GRE/SWI imaging is highly sensitive to susceptibility variations that accompany the

intraparenchymal hemorrhage.

Subacute infarction is characterized by increased mass effect, T2 shine through

effect on DWI, cortical enhancement on T1C+ and cortical laminar necrosis on T1WI.

Chronic infarction is characterized by T2WI/ FLAIR hyperintense signal with

atrophic changes.

DWI and perfusion WI techniques will help in assessing any hyperacute

ischemic changes. DWI and ADC image are read together, hyper intensity on DWI

and hypointense signal on ADC of the corresponding area is suggestive of acute

29
infarction.

Danier C. et al,38 conducted prospective cohort study on 661 stroke patients out of

which 14 patients had early onset seizures. They concluded that there was a high

risk of early seizure in watershed infarcts (23%) than territorial strokes (5.3%).

GLIOSIS:39

Neuroglial cells consist of microglia, astrocytes, and oligodendrocytes. These glial

cells cells perform various functions in the brain and buffer the extracellular spaces

around neurons and presynaptic terminals against increases in the potassium ions.

Gliosis is an astrocytic (glial cells) response to tissue damage and is the end result of

various focal or diffuse central nervous system injuries including trauma, infection,

infarctions which can be focal / diffuse. The pathological changes that occur in gliosis

may impair glial control of extracellular potassium ions and lead to excessively

excitable neuronal border regions resulting in siezures.

POST TRAUMATIC EPILEPSY:40

Post traumatic epilepsy is defined as unprovoked seizures occurring at least one

week after initial trauma. The pathological mechanism includes deposition of tissue

hemosiderin which is potent epileptogenic agent.

The overall risk of post traumatic seizures is 1.8% to 5% for civilian injuries, but can

be as high as 53% for war injuries. In case of closed head injuries, the most common

sites of injury are along the inferior anterior regions of the brain because of

irregularities of the skull base at these locations – orbital surfaces of the frontal lobe,

undersurface of the temporal lobe, the frontal pole, and the temporal pole. These

30
traumatic shearing injuries of the brain, or contusions, are often associated with

hemorrhage, which eventually results in hemosiderin deposition and reparative

gliotic changes.

MR imaging is an effective modality for demonstrating diffuse axonal injury,

intracerebral hematoma, subdural hematoma, contusions, and gliosis. MR

imaging can detect evidence of old hemorrhagic lesions. Thus, MR imaging plays a

role in the management of patients with trauma and may be a helpful tool in

predicting the prognosis for the patient in the long run.

MRI features:

The characteristic findings include T2/FLAIR hyperintensity. The gliosis usually

appears as a region of hyperintensity on T2WI often associated with volume loss and

hemosiderin appears hypointense on T2 and GRE.

Anna Messori, et al41 followed 135 adult traumatic brain injury patients with serial

MRI and concluded that MRI changes of gliosis, hemosiderin accumulation may be

abler to identify the risk of post traumatic epilepsy.

VASCULAR MALFORMATIONS:42

Intracranial vascular malformations (IVMs) are spectrum of entities which involve

arteries ,veins and capillaries of brain. out of all the malformations, arteriovenous

malformations (AVMs), and cavernous malformations (CCMs) are of particular

importance for epilepsy. Seizures may occur de novo or because of intracerebral

hemorrhage. Timely imaging is thus crucial for patients with seizures and AVMs or

31
CCMs. They commonly present in the 2nd and 3rd decade. Presenting symptoms

include headache, seizures, focal ischemic neurological deficits or hemorrhage.

Arteriovenous malformations (AVM):

AVMs are congenital, developmental anomalies which consist of a tangle of

serpiginous, thin walled blood vessels without intervening capillary network. This

direct arteriovenous shunting of blood leads to focal cerebral ischemia because of

the steal phenomenon. Subclinical hemorrhage can be present in the brain

parenchyma which can lead to gliosis and hemosiderin deposition.

MRI features:

AVMs consist of feeding arteries, a central nidus and draining veins. AVM looks like

a tightly packed mass or a honeycomb of flow voids on both T1 and T2WI with focal

area of blooming on SWI or T2* images. The intervening brain parenchyma is gliotic

and is hyperintense on T2WI and FLAIR.

Cavernous malformations (CCM):

Cavernous malformations are composed of well circumscribed vascular spaces

containing blood in different stages of evolution. These are also called as

'cavernoma's. The absence of any intervening neural tissue within the lesion is the

hallmark of cavernoma.

MRI features:

The typical MRI appearance of a cavernous malformation is popcorn like with central

heterogeneous hyperintense signal on all pulse sequences, surrounded by a rim of

low signal intensity from hemosiderin. Hemosiderin results in magnetic susceptibility

32
artifacts, so, sequences which are more affected by magnetic susceptibility artifacts

will tend to have the greatest sensitivity for detecting small cavernomas. Thus, when

compared with conventional or fast spin echo sequences

, gradient echo (GRE) imag

es have a much higher sensitivity. The lesions are almost completely black on GRE

images, due to blooming artifacts. T2* and SWI significantly increase the sensitivity

of MRI to detect small cavernomas.

Cavernomas can be associated with developmental venous anomalies seen as

curvilinear flow void on coronal T2WI.

Requena et al,43 studied 47 pateints with cavernomas and described that

cavernomas have the characteristic appearance of a range of blood products. They

show central areas of high signal on both T1WI and T2WI, reflecting oxidized

haemoglobin, with darker areas on T1WI due to deoxyhaemoglobin. The ring of

surrounding hemosiderin appears dark on T2WI. Calcification, if preesent, usually

appears dark on both T1WI and T2WI.29

Hakan Kayali et al,44 studied 37 patients with cavernoma on MR imaging

30 male and 7 female patients concluded that 57% of the patients showed

supratentorial location of the lesions.

Moran NF et al.45 performed a systematic review and concluded that frontal lobe

cavrenomas have a higher incidence of GTCS than other locations.

Current study had a patient presented with GTCS and was diagnosed to having

cavrenoma in right frontal lobe.

33
MESIAL TEMPORAL SCLEROSIS (MTS):46

Mesial temporal lobe sclerosis (MTS), also known as hippocampal sclerosis, is

characterized by atrophy of the hippocampus and other adjacent structures. It is the

most common cause of localization-related epilepsy. The most common

manifestation of MTS is temporal lobe epilepsy (TLE), which is the most common

form of complex partial seizures (CPS). Intractable temporal lobe epilepsy is seen in

60% to 80% of cases. The pathology includes neuronal cell loss, gliosis, and

sclerosis within the mesial temporal lobe.

MTS is usually unilateral but can be bilateral in up to 20% of cases; however,

symptoms may be unilateral depending on the side most affected. In 80% of cases,

one side is more severely affected than the other. Patients classically present with

CPS lasting one to two minutes. Preceding auras like epigastric “rising” sensations,

fear, anxiety, and autonomic symptoms are common. Freezing spells, altered

consciousness, and automatisms are typical and sometimes accompanied by motor

symptoms like dystonic posturing. Secondary generalization is rare; but,

disturbances of cognition, language, memory, and mood may occur postictally.

MRI features:47

The coronal T2WI and FLAIR are most sensitive for detecting medial temporal

sclerosis.

Primary signs:

 Small atrophic unilateral hippocampus with loss of internal architecture and

loss of normal digitations of the head.

 Hyperintensity on both T2WI and FLAIR images.

34
Secondary signs:

 Ipsilateral atrophy of the mamillary body, fornix columns (Papez circuit), and

amygdala.

 Atrophy of ipsilateral collateral white matter bundle.

 Increased T2WI signal in the ipsilateral anterior temporal lobe white matter

with loss of grey-white matter demarcation.

 Unilateral dilatation of the temporal horn (less reliable).

Quantitative (volumetric) MR imaging: T1W 3D volume acquisitions are helpful in

quantitative evaluation of hippocampal volume, which increases the sensitivity over

visual analysis for detection of hippocampal sclerosis. Manual tracing of the

hippocampus is done, and measurement is taken. The normal hippocampal volume

is approximately 2.8 mI.

T2 Relaxometry (mapping): It gives the objective measure of the T2 relaxation time

in the hippocampus. A series of T2WIs are acquired in the same slice using different

TEs and the decay in signal intensity is measured.

MR Spectroscopy: Decreased NAA/ creatinine or decreased NAA/ creatinine+

choline ratios signifiy neuronal loss and metabolic dysfunction. A decrease in these

ratios is shown to be of good value in lateralizing temporal lobe epilepsy in patients

with bilateral temporal lobe structural abnormalities.

Van Paesschen W. et al.,48 studied 40 patients with intractable temporal lobe

epilepsy as a part of the presurgical evaluation, using T2 relaxometry and volumetry

of hippocampus. Hippocampal volume asymmetry could reliably be detected on

visual inspection of the MRI with the hippocampal volume ratio of 0.85 or less. It was

concluded that Quantitative MRI is reliable for detecting Hippocampal Sclerosis.

35
MALFORMATIONS OF CORTICAL DEVELOPMENT:

Cortical malformations are commonly identified as causes of epilepsy and

neurodevelopmental deficits. Neuroimaging Commission of the International League

against Epilepsy subdivided malformations as follows:49

 Diffuse cortical malformations: microcephaly, megalencephaly,

microdysgenesis, agyria, pachygyria, polymicrogyria.

 Focal or multifocal cortical malformations: hemimegalencephaly, focal

cortical dysplasia, focal polymicrogyria, tuberous sclerosis.

 Heterotopias.

Barkovich et al. 50 updated the classification of MCDs in 2012 and divided them into

three basic categories:

Group I: Malformations secondary to abnormal neuronal proliferation or apoptosis

Group II: Malformations secondary to abnormal neuronal migration

Group III: Malformations secondary to abnormal postmigrational development

Of all these malformations, three are more commonly associated with epilepsy.

1) FOCAL CORTICAL DYSPLASIA (FCD):51 FCD is one of the most common

causes of epilepsy attributable to focal cerebral dysgenesis. Three types of FCDs

are recognized, with type II being the most common. Type I and III are grouped

under group III (postmigrational MCD), while type II is grouped under group I. FCD is

one of the most common causes of medically refractory epilepsy. 60% FCDs are

found involving temporal lobes.

MRI features:

36
  Cortical thickening noted on at least three or more contiguous slices.

 Blurred of gray-white matter junction

 A wide or deep sulcus, with thickened gray matter

 Linear/ curvilinear/ funnel-shaped tapering of abnormal T2/FLAIR signal

intensity extending from the cortical white matter junction to the ependymal

surface of the lateral ventricle

 Transmantle sign – almost exclusive to FCD type II

2) LISSENCEPHALY:51 Lissencephaly is a rare congenital malformation due to

abnormal neuronal migration. It means „smooth brain‟ and includes a spectrum of

malformations from the total failure of development of cerebral gyri and sulci to the

development of coarse, broad flat gyri with shallow sulci. Clinically presentation

includes microcephaly, mental retardation, hypotonia., feeding problems and

seizures.

MRI features:

 Smooth cortical surface, a thick band of deep GM that is sharply demarcated

from the underlying WM, and large ventricles – classic lissencephaly

 A band of smooth grey matter separated from a relatively thicker, more

gyriform cortex by a layer of normal-appearing white matter – ‘band

heterotopia’ (double cortex syndrome)

 Smooth interface between gray and white matter with lack of normal pattern of

interdigitations.

3) POLYMICROGYRIA:51 It is a malformation due to abnormal postmigrational

37
development giving rise to irregular cortex with numerous small convolutions and

shallow or obliterated sulci. It may be unilateral or bilateral and is characterized by

numerous small gyri with predilection for sylvian fissure. It can be associated with

atrophy (predominantly posterior) and anomalous venous drainage.

MRI features: Thickened or overfolded cortex with nodular surfaces and poorly

developed sulci, irregular "stippled" gray-white matter interfaces are the

characteristic findings.

Lehericy et al.,52 studied 222 patients with temporal lobe epilepsy, using MRI, and

the abnormalities detected were FCD, nodular heterotopia, abnormal gyri,

hippocampal malformations (7%) and concluded that MRI plays a crucial role in

temporal lobe epilepsy imaging.

NEUROCUTANEOUS SYNDROMES: Neurocutaneous syndromes that commonly

manifest with seizures are Tuberous Sclerosis and Sturge Weber Syndrome.

TUBEROUS SCLEROSIS:53

It is a systemic disease of autosonmal dominant inheritance with prominent CNS

and cutaneous manifestations. A classic triad is defined consisiting of adenoma

sebaceum, epilepsy and mental retardation. Cortical hamartomas called "tubers",

which are similar to cortical dysplasia are charecterstic of TS. Subependymal

nodules are small lesions that protrude into the lateral ventricles. These nodules may

sometimes be calcified.

Literature suggests that more than 80% of patients with tuberous sclerosis develop

seizures during childhood. Many initially manifest infantile spasms (characterized by

38
a sudden jerk with flexion at the waist and raising of the arms) during infancy.

Alternatively, other seizure types can also occur, such as focal/partial seizures

(involving part of the body or altered awareness with abnormal electrical activity in a

specific area of the brain) or generalized seizures (whole body convulsions or drop

attacks with abnormal electrical activity throughout the brain).

MR imaging features:

T1 and T2 signal abnormalities vary depending on the degree of myelination.

Cortical and subcortical tubers – in infants, these are noted as regions of T1

hyperintensity and T2 hypointensity, but after about 6 months of age, the SI

characteristics are reversed because of myelin maturation.

Subependymal nodules – small nodular bumps protruding from ventricles. In

unmyelinated brain, these are T1 hyper and T2 hypo intense; with progressive

myelination, they become isointense to white matter. When calcified, they are hypo

on T1 and T2WI with blooming on T2* GRE images.

Subependymal giant cell astrocytomas (SEGAs) – Circumscribed astrocytic

tumors that occur along the ventricular ependymal (vast majority are found near the

foramen of Monro). SEGAs have mixed SI on both T1 and T2WI with strong

heterogeneous enhancement on T1 C+ images.

Rima Nabbout et al,54 in TOSCA, a multicenter, international disease study

designed to collect data, retrospectively and prospectively, on patients with TSC

from several countries, studied 2216 eligible patients and concluded that 1852

patients (83.6%) had seizures out of which 1250 patients (67.5%) had focal seizures.

39
STURGE-WEBER SYNDROME:55

Sturge-Weber syndrome is a sporadic (i,e. not familial or not inherited), congenital

segmental vascular neurocutaneous syndrome characterized by various vascular

malformations. These include ipsilateral facial angioma in the distribution of the

trigeminal nerve (a dermal capillary-venular malformation causing port-wine

birthmark), retinal choroida algioma (with or without glaucoma) and cerebral

capillary-venous leptomeningeal angioma. Clinical presentation includes port wine

birth mark, intractable seizures, hemiparesis, hemianopsia and mental retardation.

Intractable epilepsy is the earliest and the most common clinical presentation in

these patients. They are usually focal (partial) motor seizures, usually characterized

by jerking of one side of the face or limbs, or both. The seizures may become

generalized. Some children may have Other types of seizure like atonic seizures

(drop attacks), myoclonic jerks, infantile spasms are also not uncommon.

MRI features:

 Volume loss of the ipsilateral (angioma side) cerebral hemisphere with

enlargement of subarachnoid spaces.

 Serpentine FLAIR sulcal hyperintensities - ivy sign

 Pial angiomata with serpentine enhancement covering the underlying gyri,

extending deep into the sulci on T1 C+ images

 Dystrophic cortical/subcortical calcifications seen as linear T2 hypointensities

and bloom on SWI/ T2* GRE.

 Enlarged and elongated eyeball.

Schmauser I et al56 studied 4 children with SWS, aged 7, 9, 11 and 19 months and

concluded that MRI is the method of choice to detect intracranial involvement in

40
SWS.

NEOPLASMS:57

Neoplasms are the structural epileptic substrate in about 4% of patients with epilepsy

in the general population. The temporal lobe is most common location for tumors

presenting with seizures (68%). Based on histopathological features, WHO classified

brain tumors into four grades i,e. Grade I to Grade IV. Grade I and II are referred as

low grade and Grade III and IV are referred as high grade. Among brain tumors, low

grade gliomas, glioneuronal tumors including gangliogliomas and dysembryoplastic

neuroepithelial tumors (DNETs), are most likely to present with seizures. Low grade

gliomas causing seizures include pleomorphic xanthoastrocytoma (PXA) and

oligodendroglioma.

Pleomorphic xanthoastrocytomas (PXAs) are WHO Grade II tumors which are

superficially located solid cystic masses adjacent to the leptomeninges. The most

common location is the temporal lobe. The solid component of the tumor is

hetrogenoeusly hypo to iso intense to cortex on T1WI. The cystic component is

hyper intense to CSF on T2WI. Most of the tumors show a hyperintense nodule on

T2/FLAIR images and the nodule enhances on T1C+ images. Leptomeningeal

involvement is characteristic of this tumor.

Oligodendrogliomas are WHO Grade II tumors which are usually peripherally

located and commonly seen in the frontal or temporal lobe. They display gyriform

calcifications and adjacent changes in the calvaria. They are hypointense on T1WI

and heterogenously hyperintense on T2/FLAIR images with marked cortical

41
thickening. Contrast enhancement is variable and is seen in about one half of the

cases. GRE images may show linear/ nodular tumoral calcification as foci of

hypointensity.

Gangliogliomas are WHO Grade I glioneural tumors and they are most commonly

seen in the temporal lobe. Most of the patients are younger than 30 years.

They are solid cystic lesions that are cortically based, with minimal or no mass effect.

Peritumoral edema is generally absent. Calcification is often present. These tumors

can be associated with focal cortical dysplasia adjacent to them. These are

hypointense on T1WI and hyperintesne on T2 WI and show variable enhancement

on T1 C+ images, ranging from none or minimal to moderate but heterogeneous

enhancement.

Dysembryoplastic neuroepithelial tumors (DNET) are WHO Grade I tumors which

are primarily seen in children and young adults. These are cortical based benign

tumors with characterstic multicystic/ multinodular/ multilocular/ „bubbly‟ appearance.

They are strikingly hyperintense on T2WI with multiloculated appearance with no

peritumoral edema. They generally show little or no enhancement on T1 C+ images.

MRS shows decreased NAA without elevated Cho or Cho:Cr ratio.

MENINGIOMA:

Meningioma is the most common primary non glial intracranial tumor. It is one of the

few brain tumors that exhibit a female predominance. Most common location of the

meningiomas is parasagittal followed by cerebral convexities. They are extra axial

dural based tumors that can show arterial encasement, venous sinus invasion, and

42
marginal extension.

MRI features:

The tumor is iso to hypointense to cortex on T1WI and hyperintense on T2WI. A

CSF-vascular "cleft" is noted on T2WI as a hyperintense rim interposed between the

tumor and brain with number of "flow voids" representing displaced vessels within

the cleft. The calcifications are hypointense on both T1 and T2 WI. The tumor may

show bony erosion or hyperostosis. Most of the meningioma]s don‟t restrict on DWI.

On T1C+ images, it shows intense homogeneous enhancement and a dural tail

representing reactive dural thickening can be seen in many cases.

Marta Maschio et al,58 studied 808 patients (447 men, 361 women) who had at least

one seizure. Focal seizures were the most frequent type (57.6%) with impairment of

consciousness in 42.3%. They concluded that the most common tumor associated

with epilepsy was glioblastoma (268 patients, 33.1%), followed by atypical

meningioma (139 patients, 17.2%) and metastases (88 patients, 10.9%). Most

common sites of involvement were frontal lobe (284 patients, 35.2%) and temporal

lobe (158 patients, 19.6%). Multiple sites were involved in 250 patients (30.9%).

Simple partial seizures were the predominant type in patients with parietal (63.1%),

occipital (50.0%) and frontal (48.4%) lesions. Complex partial seizures were

commonly seen in patients with temporal lesions (46.4%). Simple partial seizures

were the most common type in patients with multisite lesions (57.2%). Status

epilepticus occurred in only 32 patients (4.0%) and was non convulsive in 24 (3%).

HYPOXIC ISCHAEMIC INJURY (HIE):59

Antenatal or perinatal or post-natal vascular events like hypoxic, anoxic, ischaemic,

43
haemorrhagic cerebral injuries can cause a wide spectrum of intracranial

abnormalities, some of which may be associated with seizures/ epilepsy. The lesions

can be unilateral or bilateral; if bilateral, they can be with and without symmetry.

Unilateral abnormalities may include focal haemorrhage

and porencephaly .

Perinatal HIE is a common cause of epilepsy and the features depend on the

severity and timing of the injury.

MRI features: It shows periventricular leucomalacia, multicystic encephalomalacia

and brain stem and basal ganglia changes that typify varying degrees of hypoxic

ischaemic injury. DWI confirms the diffuse restriction.

CEREBRAL ABSCESS:60

Pathogens growing within the brain parenchyma, initially cause cerebritis and then

eventually demarcate into a cerebral abscess. Causes include direct extension of

infections, haematogenous spread, direct introduction by trauma or surgery. Risk

factors for haematogenous spread are bacterial endocarditis, congenital heart

diseases, lung infection, dental abscess and systemic sepsis.

MRI features:

MRI is a sensitive modality for the detection of cerebral abscesses with MRS and

DWI adding more specificity to it. T1WI shows central low intensity (hyperintense to

CSF) with peripheral low intensity (vasogenic oedema). T2 WI shows central high

intensity (hypointense to CSF, does not attenuate on FLAIR) with peripheral high

intensity (vasogenic edema). The abscess capsule may be visible as slightly low

44
signal thin rim. Central diffusion restriction on DWI with low signal on ADC is

characteristic feature. On contrast administration, it shows ring enhancement.

Ventriculitis may be present, which may cause hydrocephalus. Elevation of a

succinate peak on MRS is relatively specific but not present in all cases. Other

findings include high lactate, alanine, leucine, isoleucine and valine peaks with

reduced NAA peak.

CEREBRAL VENOUS THROMBOSIS (CVT):61

CVT includes thrombosis of dural venous sinuses, superficial cortical veins, deep

cerebral veins. Common predisposing factors are pregnancy, puerperium, infection,

oral contraceptive, coagulopathies, tumors, and trauma. Headache, seizures and

nausea are the most common symptoms in most of the patients. Superior sagittal

sinus is the most commonly thrombosed dural sinus followed by transverse, sigmoid

and cavernous sinuses. Subcortical, hemorrhagic venous infarcts are a common

finding in case of veno-occlusive disease. Retrograde extension of thrombous into

cortical or deep medullary veins occur in approximately 40% cases of dural sinus

thrombosis.

The MR protocol includes T1WI, T2WI, T1 contrast, MR venogram, TOF & PC.

MRI findings:62

The MR findings vary with the clot age. Acute thrombus is isointense to cortex on

T1WI, while late acute clots are hyperintense. Sub-acute thrombi are typically hyper

intense on all sequences. Sagittal 2D PC or coronal 2D TOF MR venogram is best

used to evaluate the superior sagittal sinus. MR venogram demonstrates absence of

flow related enhancement. The signal void in cortical veins or the dural sinus is

45
replaced by abnormal signal. On contrats images, filling defect with asymmetric

enhancement of nearby vessels is seen.

F Masuhr et al63 studied 194 patients with acute cerebral venous thrombosis and

concluded that early symptomatic seizures were found in 86 patients (44.3%) and

status epilepticus occurred in 11 patients (12.8%).

METHODOLOGY

Study design: Descriptive study

Sample size: 100 to 150 (final sample was less because of COVID 19 situation)

Inclusion criteria:

 Patients with clinically diagnosed new-onset seizures who came to the

department of radiology, MIMS, for MRI evaluation of brain, irrespective of

age/ sex.

Exclusion criteria:

 Contraindications to MRI studies, such as patients with pacemakers, metallic

implants, aneurysmal clips.

 Claustrophobia or anxiety disorders exacerbated by MRI.

 Inability/ unwillingness to provide consent.

Study duration: 2 yrs (Jan 2020 – Nov 2021)

Procedure:

 The patients selected for the study were clinically diagnosed cases of

seizures as per ILAE 1981 criteria with the addition of febrile seizures.

46
  Informed consent was obtained from every subject or from parent/ guardian if

the subject was a minor.

 A detailed history was taken and clinical examination was done.

 Detailed neurological examination was done to find any neurological deficit.

 Based on the history and examination, a clinico-etiological diagnosis was

made.

 All the patients underwent routine investigations: Hb, TLC, DLC, ESR, urine

routine examination, blood urea, sugar, serum creatinine, serum calcium, liver

function tests, fundus examination and X-ray chest – PA view.

 All the patients undergoing MRI scanning were briefly explained about the

procedure including the risks of contrast administration.

 Patients were then subjected to different MRI sequences as per the protocol

using Philips Ingenia 1.5-Tesla unit system

Materials:

 Whole body MRI scanner Philips Ingenia 1.5-Tesla

 Contrast media: OMNISCAN (Gadodiamide)

 Emergency drugs like Inj. AVIL, Dexamethasone, and Adrenaline etc.

 Syringes 5ml, 10ml and 20 ml.

MRI Protocols -

Standard brain protocol: T1W axial & sagittal, T2W axial & coronal, FLAIR axial,

diffusion weighted imaging/apparent diffusion coefficient (DWI/ADC) and

susceptibility weighted image (SWI).

Dedicated epilepsy protocol: In addition to standard protocol, T1W IR, T2W,

47
FLAIR coronal oblique (perpendicular to the long axis of hippocampus) sequences

and T1W 3D TFE sequence are acquired. Contrast-enhanced MRI, TOF MRA, PC

MRV and MR spectroscopy were performed wherever required.

Technique of examination:

All patients screened before entry into the MRI scanning room for ferromagnetic

objects, cardiac pacemakers, aneurysm clips etc.

Patients were examined in the supine position on the MRI machine after proper

positioning and immobilization of the head was obtained and a head coil was used

for the scan.

Initial topogram of the head was obtained and sequences were planned according to

the MRI seizure protocol.

MRI protocol at 1.5T includes the entire brain from nasion to inion, conventional

routine 5mm slice thickness, T1 and T2 axial sequences, 1.5 mm slice thickness

coronal oblique T1 weighted images. 1.5mm slice thickness – are acquired as a 3

dimensional (3D) volume, there by post processing and reformatting images into

multiple planes.

Protocol also includes coronal and axial FLAIR sequences with 2-3 mm slice

thickness and 1 mm inter slice gap. A conventional thin slice, T2 weighted axial and

coronal sequence is also obtained.

Gadalonium based paramagnetic contrast agent OMNISCAN (Gadodiamide) was

used with dosage of 0.2 mL/kg (0.1 mmol/kg) if a tumor like mass lesion or vascular

malformation was identified and in cases of neurocutaneous syndromes.

As a precautionary measure, resuscitation apparatus and emergency drugs were

kept ready.

48
Every effort was made to make sure of high quality scans and to avoid artifacts.

MRI findings were recorded in all patients as per the proforma.

Statistical analysis: Statistical analysis was done using SPSS v21 for windows 10

OS. Chi square test was used for nonparametric data and t-test was used for

parametric data.

49
DISCUSSION

Seizures/ epilepsy can have a wide range of etiological factors, some of which

can be effectively managed with medical and/or surgical approaches. Patients

presenting with seizures should be thoroughly evaluated clinically. The semiology of

the seizure would be helpful in classifying the seizure into a particular type, which

helps in the treatment of the patient. Presence of any structural brain lesion/ cause

can change the entire course of management and hence patients presenting with

seizures need to be evaluated with a reliable neuroimaging modality. Out of all the

neuroimaging modalities available, MRI is proven to be a reliable and affordable tool

to identify any structural brain lesion. Patients presenting with seizures can have a

wide range of MR Imaging abnormalities based on the etiology, which will help in

planning the treatment. The current study was done to study the spectrum of MRI

findings in patients presenting with seizures and to evaluate MRI positivity in various

types of seizures. The study was designed as a descriptive study to be conducted

over a period of 2 years in Maharajah‟s Institute of Medical Sciences, Nellimarla,

Vizianagaram, Andhra Pradesh with an expected sample size of 100 to 150. The

sample constituted patients clinically diagnosed with new onset seizures, who came

to the department of radiology, MIMS for MRI evaluation of brain. Patients with

pacemakers, metallic implants, aneurysmal clips, claustrophobic patients, patients

with anxiety disorders exacerbated by MRI, patients who are unable/ unwilling to

provide consent were excluded from the study.

Although it was intended to evaluate at least 100 cases, because of the

unfortunate COVID 19 pandemic situation, only a sample of 62 patients could

be obtained. All 62 patients with clinical diagnosis of seizures were selected as per

50
the criteria laid down by ILAE 1981 with addition of febrile seizures. The clinical

history of each patient was recorded and all underwent routine biochemical

investigations as per proforma. MRI scan was carried out with 1.5T PHILIPS Ingenia

MRI scanner, employing a dedicated epilepsy MRI protocol with additional

sequences/contrast study wherever necessary. Images were studied under the

guidance of experienced faculty and the lesions/ diagnoses were charted.

Age and Sex distribution:

The age range of patients was from 1.5years to 75 years. Males were 36

(58.06%) and females were 26 (41.94%). The sample had a slight male

predominance and maximum number of patients were between 1 and 45 years

of age. Most of them were in the third decade. (12 cases)

Types of seizures:

Out of 62 patients presented with seizures, 43 patients had GTCS (69.35%), 10

patients had Complex Partial Seizures (16.13%), 5 patients had Simple Partial

Seizures (8.06%), 2 patients had Absence Seizures (3.23%) and 2 patients were

diagnosed to be having Febrile Seizures (3.23%). GTCS were the dominant type of

seizures in the sample.

MRI positivity:

The MRI examination was negative in 20 patients while it was positive

and had pathological findings in 42 out of 62 patients (67.74%), which is

statistically significant. MRI positive diagnoses (in the order of frequency) were:

Infarct

51
 Neurocysticercosis (NCC)

Tuberculoma

Gliosis

Meningioma

Venous thrombosis (CVT)

Malformations of Cortical Development (MCD)

Tuberous Sclerosis (TS)

Mesial Temporal Sclerosis (MTS)

Cavernoma

Cerebral abscess

Glioma

Sturge-weber syndrome (SWS)

Sequelae of Neonatal HIE

Cerebral infarcts:

10 patients (16.13%) revealed cerebral infarction on MRI study. Most of

them presented with GTCS with exception of 2 patients who had partial

seizures, one with simple partial seizure (SPS) and other with complex partial

seizure (CPS). Out of 10 patients, 5 patients were diagnosed with acute infarct

based on diffusion restriction on DWI and mild swelling of brain parenchyma

with effacement of adjacent sulci. 2 cases showed intraparenchymal

hemorrhage were likely hemorrhagic infarcts. Hemorrhage was iso to

hyperintense on T1WI, hyperintense on T2/FLAIR images and associated with

mild to moderate perilesional edema with adjacent sulcal effacement. (Fig.x)

3 cases were diagnosed as acute to subacute infarcts. All of them were ischemic

52
strokes; there was no evidence of any hemorrhage. They were hypointense on

T1WI with hyperintense cortical laminar necrosis and hyperintense on T2/FLAIR,

with diffusion restriction on DWI. (Fig.x)

Neurocysticercosis:

6 patients showed evidence of neurocysticercosis (NCC). All patients had

parenchymal form of NCC, with ring enhancing lesions in cerebral hemispheres.

Lesions show T1 hypo intense and T2 hyper intense contents. Few lesions

showed perilesional edema. Most of lesions were seen in parietal and frontal

lobes and some showed cystic signals with an eccentric speck within the lesion.

MRS showed choline peak in all patients.

2 patients had few ring enhancing lesions with perilesional edema (Fig.)

and 4 patients had multiple intra parenchymal lesions of different stages.

Out of 6 patients, 3 patients had GTCS, 2 patients had simple partial

seizure (SPS) and 1 patient presented with complex partial seizure (CPS). The

nature of partial seizures was relatable to the location of NCC lesions.

Tushar B. Patil, Madhuri M. Paithankar,64 studied 40 patients with probable

diagnosis of NCC and concluded that 72% patients showed one lesion, 27% with

multiple lesions and common site was parietal lobe. The results of the current study

are partially in concordance with the study done by Tushar B. Patil, Madhuri M.

Paithankar,64 in that most of the lesions were located in parietal lobe.

Tuberculoma:

Four patients had findings suggestive of tuberculoma on MRI scan. The

lesions were well defined, rim enhancing, conglomerate with thick walls of

53
different sizes. The lesions showed some perilesional edema and on MRS

revealed elevated lactate, lipid peak.

Diagnosis of tuberculoma was based on MRI appearances along with a

history of taking ATT in past or any evidence of tuberculosis in X-ray chest or

any history suggesting possible contact with a tuberculosis patient.

Out of 4 patients, two patients presented with GTCS, one with CPS and

another one with SPS. The patient who presented with CPS had a lesion

located in right frontoparietal lobe (Fig.) and the patient presented with SPS had

lesion located in left frontal lobe. The location of tuberculoma had corresponded

with the seizure semiology in case of partial seizures. Two patients who

presented with GTCS had multiple tuberculomas, probably explaining the

generalized nature of seizures.

Gliosis:

Three patients on MRI showed gliosis which is characterized by FLAIR

hyperintensities adjacent to an encepahalomalacic brain, suggesting previous brain

parenchymal insult. All three patients presented with GTCS. Out of them, one

patient showed ill-defined FLAIR hyperintensity in left temporo-parietal lobe

associated with volume loss and severe susceptibility artifact - suggesting gliosis as

a sequel of previous intra-parenchymal hemorrhage.

Another patient showed FLAIR hyperintense signal in left frontoparietal lobe adjacent

to the dilated left lateral ventricle and the lesion showed no diffusion restriction on

DWI, had high signal on ADC - suggesting gliosis as a sequel of a chronic infarct.

(Fig.)

54
Meningioma:

Meningioma was diagnosed in 3 patients. 2 of them had GTCS and 1 had SPS. MRI

of the patient who had SPS showed a well-defined, extra axial, dural based lesion

which was isointense to grey matter on both T1WI and T2WI in left frontal convexity

with significant perilesional edema causing mass effect and midline shift. The lesion

showed homogeneous enhancement on contrast administration and there was mild

hyperostosis of adjacent bone (Fig.) No blooming was noted on SWI. All the features

were suggested of meningioma of left frontal convexity. The simple partial seizures

which are of motor type are explainable by the location of the lesion.

Other 2 patients who presented with GTCS had homogenously enhancing lesions

with dural tail sign and the lesions were compressing the underlying cerebral

parenchyma and causing midline shift and perilesional edema.

Cerebral Venous Thrombosis (CVT):

Three patients showed MRI features of cerebral venous thrombosis (CVT). All

three patients presented with GTCS. Out of three patients, two were female

patients who were in puerperium and showed superior sagittal sinus thrombosis.

The other patient showed a large area of T1 hypointensity which was

predominantly hyperintense on T2WI/FLAIR with serpiginous cortical

hypointensity and edema involving right corona radiata, right centrum semiovale,

right parietal lobe and minimally extending into the right posterior frontal lobe

causing partial effacement of right lateral ventricle, right sided cerebral sulci,

midline shift to left. It showed focal areas of diffusion restriction with blooming on

55
SWI. Small T1 hyperintensity with minimal prominence of the cortical vein was

noted adjacent to the edema. Phase Contrast MR Venogram (PC MRV) showed

partial loss of flow-related enhancement in superior sagittal sinus. – features

suggested partial thrombosis of superior sagittal sinus with venous hemorrhagic

infarct involving right parietal lobe, minimally extending into the right posterior

frontal lobe. (Fig.)

Malformations of Cortical Development:

Two patients were diagnosed as Malformations of Cortical Development based on

MRI features. One patient had GTCS while the other one had CPS.

In the patient with GTCS, MRI revealed pachygyria with focal area of polymicrogyria

in right frontoparietal, temporal lobes and right sylvian fissure with dilated

subarachnoid spaces. (Fig.)

In the patient with CPS, MRI revealed cortical thickening with mild irregular bumpy

cortical surface and hypo sulcation in bilateral frontal lobes and bilateral peri-sylvian

region involving parietal lobe along with inferior vermian hypoplasia.

Jagruti P et al.65 studied 76 children with seizures and CNS

malformations based on MRI neuroimaging and concluded that 19 cases

revealed corpus callosal dysgenesis, 9 patients lissencephaly and 9 focal

cortical dysplasia, 6 pachygyria, 3 polymicrogyria, 15 tuberous sclerosis and 3

Sturge Weber syndrome.

Tuberous sclerosis:

2 patients with clinical diagnosis of tuberous sclerosis, one presented

56
 with GTCS and one with CPS underwent MRI brain, which showed multiple ill-

defined areas of altered signal intensity affecting different areas of cortex and

sub cortical white matter of both cerebral hemispheres suggestive of cortical,

subcortical tubers. (Fig.)

Mesial Temporal Sclerosis:

2 patients were diagnosed with mesial temporal sclerosis with MRI showing reduced

hippocampal volume and increased T2 signal. (Fig.) The findings were unilateral in

both the cases. Both patients presented with CPS typical of temporal lobe seizure. It

is in agreement with the known fact that MRI can diagnose MTS in almost all cases.

Cavernoma:

2 patients were diagnosed to be having cavernoma (One patient in left temporal

lobe, another in right frontoparietal lobe) and both of them presented with GTCS.

Patients showed well defined T1 hyperintense lesion with irregular margins

(popcorn like appearance), which is T2/FLAIR hyperintense with hypointense rim

and showed hemorrhagic signal intensities with blooming on SWI. (Fig.)

Cerebral abscess:

The diagnosis of cerebral abscess was made in 2 patients, out of whom,

one patient had GTCS and the other one had CPS.

The patient who presented with GTCS showed evidence of space

occupying lesion involving left frontoparietal cortex with extensive perilesional

edema with low signal intensity on T1W image and high signal intensity on T2W

image with peripheral hyperintensity on T1WI. The lesion showed central

57
diffusion restriction on DWI and rim enhancement on contrast administration.

MRS on the lesion showed high lipid, lactate peak. (Fig.)

58
The patient who presented with CPS showed well defined lesion in right frontal lobe

which has peripheral low signal and central high signal on T2WI with mild to

moderate perilesional edema. The lesion showed central diffusion restriction on DWI

and ring enhancement on contrast administration. The seizure semiology was of

motor in nature, explaining the probable origin in frontal lobe, where the lesion is

located.

Glioma:

One patient was diagnosed to be having low grade glioma based on MRI

features and he presented with GTCS. Patient showed a well-defined rounded

lesion left frontal lobe. The lesion was isointense to cortex on T1WI and

hyperintense on T2W & FLAIR images with no evidence of diffusion restriction or

blooming on SWI. The lesion was causing mild mass effect and some midline

shift to right. The lesion showed no contrast enhancement and MRS showed

elevated choline peak. (Fig.)

Sturge-Weber Syndrome:

One patient revealed MRI features suggestive of Sturge-Weber syndrome

and the clinical presentation was complex partial seizures (CPS). On MRI, focal

cortical atrophy in right frontoparietal and occipital lobes was noted with

predominant involvement of occipital lobe. On contrasts administration, Intense

pial enhancement was noted in these regions. (Fig.). Predominant involvement

of occipital lobe can probably explain the seizure semiology which involved

visual aura.

59
Sequelae of Neonatal HIE:

3year old female child presented with GTCS, on MRI, revealed extensive and diffuse

T1 hypo, T2 hyper, FLAIR hypointensity with poor grey white matter differentiation

and without any evidence of restricted diffusion. Large periventricular cysts with

moderate ex-vacuo dilatation of lateral ventricles, atrophic bilateral caudate nuclei

and thalami and grossly thinned out corpus callosum are also noted. (Fig.). Birth

history of the baby revealed that it was a term baby with delayed cry and very low

APGAR score. MRI findings in correlation with birth history suggest that the findings

are sequelae of perinatal cerebral hypoxic injury.

Etiological distribution of MRI findings:

On an etiological basis, vascular causes (Infarcts and venous thrombosis)

constituted the most common MRI abnormality closely followed by infectious causes

(NCC, Tuberculoma and Cerebral abscess) in patients presenting with seizures.

These results only signify that the probability of detecting lesions of vascular and

infective etiology is more in case of seizures. But it cannot be concluded that infarcts

and infections have the highest epileptogenic potential, because the sample

collected was patients having seizures and not the patients with particular lesions.

To evaluate the epileptogenic potential of various brain lesions, age /sex matched

patients having various brain lesions should be collected and the incidence of

seizures should be studied in them. The current study is in agreement with many

similar studies conducted in India but slightly differs with some studies.

Dr. Kumar Ashok Charan et al16 studied 72 patients with seizure disorder

60
who underwent MRI in Department Of Radiology, Bokaro General Hospital, Bokaro,

Jharkhand and the examination revealed pathological findings in 31 out of 72

patients which included, Stroke (22.5%), Mesial temporal sclerosis (22.5%),

Infections (16.1%), Developmental disorders (12.9%), tumors/vascular abnormalities

(19.3%) and Phacomatosis (6.4%). The study concluded that MRI play a significant

role in patients presenting with seizures and helps to identify the cause of the

seizures.

The results of the current study are in concordance with the above mentioned study

by Dr. Kumar Ashok Charan et al16 in that the most common abnormal MRI

diagnosis in patients presenting with seizures was stroke.

Rajashekhar Muchchandi, Nandini Takalaki26 studied 60 seizures patients with

MRI in a tertiary care hospital, Karnataka, and the MRI positivity was 50%. The findings in

the order of frequency were cerebral infarct with gliosis (20%), NCC (6.66%), atrophy

(6.66%), gliomas (1.66%), cortical malformations (3.34%),tuberculoma (3.34%),

venous thrombosis (3.34%), cavernoma (3.34%), meningioma (1.66%). They

concluded that cerebrovascular causes (infarct with gliosis, venous thrombosis)

constitute (21.64%) the most common MRI diagnosis in patients presenting with

seizures.

The results of the current study are in concordance with the above mentioned study

by Rajashekhar Muchchandi, Nandini Takalaki26 in that the most common

abnormal MRI findings in patients presenting with seizures were of vascular etiology.

Ponnatapura J et al.,22 who studied 129 patients of new-onset seizures with

both MRI and electroencephalography (EEG) concluded that MRI could detect

61
potentially epileptogenic lesions in 59 patients (47%) and the frequency of

epileptogenic lesions was highest in patients who had focal-onset seizures (81%).

The most common lesion type was infection and inflammation (28%), with

neurocysticercosis being the most common, followed by mesial temporal sclerosis,

ischemia, and tumor.

The current study differs with Ponnatapura J et al.22 study to a very slight extent, in

that the dominant etiology leading to seizures based on abnormal MRI findings in the

current study was of vascular origin. However it was closely followed by infectious

etiology. The predominant lesion of infectious etiology is however the same in both

the studiers i,e. neurocysticercosis. Both these studies are also in agreement about

the most common type of seizures that can have a MRI demonstrable lesion i,e.

focal/ partial seizures.

Amritpal Singh Multani et al15 studied 250 patients with focal seizures with

exclusion of idiopathic generalized epilepsy, acute head trauma, febrile seizures, and

acute infarct/hemorrhage cases. MRI showed normal study in 108 cases (43.2%), 58

cases (23.2%) of neuroinfection, 39 cases (15.6%) of gliosis, 25 cases (10%) of

neoplasms, 15 cases (6%) of developmental anomalies, two cases (0.8%) of

Rasmussen encephalitis and hypoxic-ischemic encephalopathy and one case (0.4%)

of vascular anomaly. The study concluded that CNS granulomatous pathology

(predominantly NCC) and gliosis/ encephalomalacia were the two most common

abnormalities detected on MRI. MRI positivity was 56.8%.

The current study is in concordance with the study by Amritpal Singh Multani et

al15 in that the MRI was positive in 56.8% cases, however the cases taken were all

focal seizures. The most common cause of seizures was neuroinfection. As the

62
infarct/ hemorrhage cases were excluded by default in their study, the results of both

the studies are comparable if cases of infarctions are excluded in the current study.

After vascular causes, the second most common cause of seizures in the current

study was neuroinfection. Hence it can be said that both these studies are in

agreement with each other.

MRI positivity based on sex:

MRI positivity was more in males but it‟s not statistically significant. This is because

sex is not usually a factor that can influence an MRI finding.

MRI positivity based on age: MRI Positivity was maximum in patients >60yrs age

(85.71%) followed by 1-15yrs age group (71.43%), which was statistically significant.

This is probably because the predominat etiology in the study was infarcts, and

infarcts are more common in patients >60yrs age.

Age distribution of various MRI findings:

Infarcts were the dominant MRI diagnoses in case of both 31-45 years age group

and >60 years age group. Seizures of infectious etiology (NCC, Tuberculoma,

Cerebral abscess) were more common in patients between 16 and 45yrs of age.

Out of 30 cases between 16 and 45 years of group (16 to 30years -14 ; 30 to

45years – 16 ), total 7 cases were diagnosed to be of infectious etiology (4 cases of

NCC, 2 cases of Tuberculoma, 1 case of Cerebral abscess).

Most common etiology in children (1-15yrs group) was neuroinfections.(total 3 cases;

1 case of NCC, 1 case of Tuberculoma, 1 case of Cerebral abscess).

63
 Arti Anand et al19 studied 95 children under the age of 12 years over a period

of 2 years who presented with epilepsy and MRI showed neuroinfection (29.8%) as

the most common etiology followed by anoxia and hypoxic-ischemic

encephalopathy.

The current study is in agreement with the study by Arti Anand et al19 in that the

most common MRI diagnosed etiology in children with seizures was neuroinfections.

MRI findings in various types of seizures:

Generalized Tonic Clonic Seizures (GTCS):

Generalized Tonic Clonic Seizures (GTCS) were the dominant type of seizures in the

sample. Out of 43 cases presented with GTCS, 15 cases were normal on MRI and

28 cases revealed pathological findings on MRI with an MRI positivity of 65.12%.

Wide spectrum of imaging findings were noted including infarcts (8), NCC (3), Gliosis

(3), Venous thrombosis (3), Tuberculoma (2), Cavernoma (2), Meningioma (2), MCD

(1), Tuberous Sclerosis (1), Cerebral abscess (1), Glioma (1) and Sequelae of HIE

(1). Most of the cases were infarcts.

Complex Partial Seizures (CPS):

9 out of 10 cases of Complex Partial Seizures (CPS) turned out to be MRI positive

giving an MRI positivity of 90%. MRI diagnoses include MTS, Infarcts, NCC,

Tuberculoma, MCD and Tuberous Sclerosis. Both the cases of MTS presented with

CPS and both were diagnosed accurately on MRI.

Simple Partial Seizures (SPS):

64
All the 5 cases presented with Simple Partial Seizures (SPS) were MRI positive with

MRI positivity of 100% and epileptic substrates were accurately diagnosed in all the

cases. Diagnoses include NCC, Infarct, Tuberculoma and Meningioma. The location

of lesion was relatable with the seizure type and semiology in almost every case.

This is probably because the cause of seizures is directly related to the damage of

brain parenchyma and associated reactive changes at a specific location.

E Rahimian et al18 studied 198 patients with focal seizure out of which 127

cases (64%) had normal MRI, 21 cases (10.5 %) temporal sclerosis,15 cases (8%)

ischemia, 14 cases (7%) tumor, 8 cases (4%) gliosis, 8 cases (4%) developmental

anomaly 4 cases (2% ) focal atrophy and 1 case (0.5%) vascular anomaly.

The results of the current study are partially in concordance with the study by E

Rahimian et al18 in that MTS and infarcts were the most common diagnoses in

patients presenting with focal seizures (both SPS and CPS) in both the studies.

However, MRI positivity was way less in their study (only 36%) as compared to the

current study (90% for CPS and 100% for SPS; overall 95% for focal/ partial

seizures).

Absence Seizures (AS):

MRI didn‟t‟ reveal any abnormality in all 2 cases of absence seizures with 0% MRI

positivity. It‟s an established fact that most of the cases of absence seizures don‟t

have a significant structural abnormality demonstrable by a routine MRI scan but

advanced studies like fMRI and DTI may be able to detect some abnormalities.

Qiu W et al.66 studied 14 children (aged 6-13 years) with absence epilepsy

65
who had a normal study on routine MRI scanning and 14 healthy children

(age/ sex matched) as control group. MRI Diffusion Tensor Imaging (DTI) was used

to evaluate all the children and it was concluded that there was significant increase

of mean diffusivity (MD) and radial diffusivity (RD) in left medial prefrontal cortex

(MPFC), and decrease of fractional anisotropy (FA) in left precuneus and axial

diffusivity (AD) in both left MPFC and precuneus. Brain volumes of both groups didn‟t

show any significant difference. It was concluded that DTI can pick up abnormalities

in case of absence seizures even if the routine MRI is normal.

Febrile Seizures (FS):

MRI didn‟t‟ reveal any abnormality in all 2 cases of febrile seizures with 0% MRI

positivity. This is probably because a febrile seizure is just a manifestation due to

reduced seizure threshold of brain and not due to any particular abnormality.

Limitations of the study:

 Small sample size (final sample size was less than intended to be, because of

COVID 19 pandemic)

 Method of sampling was not random, but it was a purposive nonrandom

sampling.

 All the subjects taken were patients diagnosed with seizures and the

study doesn’t have a control group, so the results only indicate the

probability of MRI detecting a seizure causing lesion, but doesn’t

indicate the probability of an MRI detectible lesion causing seizures.

 Because of the above said reasons the results of the current study cannot be

accurately applied to general population.

66
CONCLUSION

Patient presenting with seizures warrants detailed evaluation of seizure semiology,

type, age at onset, family history, neuroimaging, so on and so forth. Neuroimaging is

invaluable in identifying, assessing and classifying any structural brain lesion that

could be responsible for seizures. Out of all the neuroimaging modalities available,

MRI is a relatively superior and has most of the characteristics that are necessary for

good diagnostic tool in terms of accuracy, accessibility and affordability. MRI is a

guiding tool in appropriate treatment of the seizures and can predict prognosis also.

Employing and reviewing the images in a systemic manner helps in the identification

of subtle epileptogenic structural abnormalities.

Current study has been done on 62 patients with clinical impression of seizures,

using MRI with appropriate imaging protocols to evaluate the spectrum of findings,

various etiologic factors for seizures, and the most common imaging abnormality.

The study revealed various vascular, infectious, neoplastic and developmental

causes that can give rise to seizures. MRI abnormalities in the order of frequency

were Infarcts (16.13%), Neurocysticercosis (9.68%), Tuberculoma (6.45%), Gliosis

(4.84%), Meningioma (4.84%), Cerebral Venous Thrombosis (4.84%), Malformations

of Cortical Development (3.23%), Tuberous Sclerosis (3.23%), Mesial Temporal

Sclerosis (3.23%), Cavernoma (3.23%), Cerebral abscess (3.23%), Glioma (1.61%),

Sturge-weber syndrome (1.61%) and Sequelae of Neonatal HIE (1.61%). The most

common MRI abnormality was cerebral infarct. Vascular etiology was the most

common MRI diagnosed cause. MRI has excellent soft tissue contrast, good spatial

resolution and multipanar imaging capability, lacks ionizing radiation and has good

accuracy. Because of these reasons MRI can be used as the first neuroimaging

67
modality in evaluation of seizure/epilepsy as it identifies the epileptogenic substrate

in most of seizure cases with a structural brain lesions/ abnormalities, even if they

are subtle. MRI could diagnose the probable causes of seizures in all cases of SPS

and in almost all cases of CPS. MRI could detect probable causes of seizures to a

moderate extent in case of GTCS and couldn‟t find any possible causes in case of

absence and febrile seizures.

It can be concluded that MRI with appropriate seizure/epilepsy protocols plays a

significant and golden role in evaluation of patients presenting with seizures/epilepsy

especially in case of partial/ focal seizures. A study with a bigger sample size is

needed to increase the power of study.

SUMMARY

The current study was conducted in a medical college located in Vizianagaram,

Andhra Pradesh. Patients clinically diagnosed with seizures and came to the

department of radio diagnosis for MRI evaluation were taken into the study with their

consent over a period of approximately 2 years. The final sample size was 62, which

was less than intended because of COVID 19 pandemic situation. MRI with

seizure/epilepsy protocol was done in all the patients; special/ additional sequences

and/or contrast administration were done wherever necessary and meticulous study

of the MRI images was done under the observation and guidance of experienced

faculty. The sample had an age range of 1.5yrs to 75yrs with male predominance.

Most of the cases presented with GTCS (69.35%). Out of 62 subjects, MRI was

normal in 20 cases while 42 cases had pathological findings with a significant MRI

positivity of 67.74%. The MRI positivity was not significantly different among male

and female subjects. The spectrum abnormalities identified on MRI were Infarcts

68
(16.13%), Neurocysticercosis (9.68%), Tuberculoma (6.45%), Gliosis (4.84%),

Meningioma (4.84%), Cerebral Venous Thrombosis (4.84%), Malformations of

Cortical Development (3.23%), Tuberous Sclerosis (3.23%), Mesial Temporal

Sclerosis (3.23%), Cavernoma (3.23%), Cerebral abscess (3.23%),Glioma (1.61%),

Sturge-weber syndrome (1.61%), Sequelae of Neonatal HIE (1.61%). MRI positivity

was 100% in SPS and 90% in CPS, implicating that MRI plays a crucial role in

patients presenting with partial onset seizures. However MRI study was essentially

normal in case of absence and febrile seizures. On an etiological basis, vascular

causes (infarcts and venous thrombosis) constituted the most common MRI

abnormality closely followed by infectious causes (NCC, Tuberculoma and Cerebral

abscess) in patients presenting with seizures. Based on the findings, despite a small

sample size, it can be concluded to an extent that MRI can significantly detect

lesions in patients presenting with seizures/ epilepsy, especially those presenting

with partial/ focal onset seizures, and can guide the treatment part. It can also be

extrapolated that MRI can be used as a follow up/ prognostic tool for the evaluation

of treatment response based on the progression or regression of lesion size,

perilesional reaction. More advanced and detailed studies with increased sample

size can further improve the accuracy of MRI as a neuroimaging modality in the

evaluation of seizures/ epilepsy.

69