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Dissertation On
DEMOGRAPHIC, CLINICAL, INVESTIGATIONAL AND ETIOLOGICAL PROFILE OF PATIENTS WITH ACUTE
SYMPTOMATIC SEIZURES
Submitted to
THE TAMILNADU DR.M.G.R. MEDICAL UNIVERSITY CHENNAI – 600 032
In partial fulfilment of regulations for award of the degree of M.D (GENERAL MEDICINE)
BRANCH- I
CHENGALPATTU MEDICAL COLLEGE, CHENGALPATTU-603001
MAY - 2018
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CERTIFICATE
This is to certify that the dissertation titled “DEMOGRAPHIC, CLINICAL, INVESTIGATIONAL AND ETIOLOGICAL PROFILE OF PATIENTS WITH ACUTE SYMPTOMATIC SEIZURES” has been prepared by Dr.A.RAJA, under my supervision in the Department of General Medicine ,Chengalpattu Medical College,Chengalpattu,during the academic period 2015-2018 ,and is being submitted to The Tamilnadu Dr. M.G.R Medical University,Chennai,in partial fulfilment of the regulations for theaward of the degree of M.D (General Medicine) and his dissertation is a bonafide work.This work has not previously formed the basis for the award of any degree.
Prof.Dr. USHA SADASIVAN M.D,Ph.D., Prof.Dr.V.R.MOHAN RAO,M.D,
DEAN, PROFESSOR & HEAD,
Chengalpattu Medical College, Department of General Medicine, Chengalpattu-603 001. Chengalpattu Medical College,
Chengalpattu-603 001.
Place:
Date:
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BONAFIDE CERTIFICATE
This is to certify that dissertation “DEMOGRAPHIC, CLINICAL, INVESTIGATIONAL AND ETIOLOGICAL PROFILE OF PATIENTS WITH ACUTE SYMPTOMATIC SEIZURES” is a bonafide work performed by Dr.A.RAJA, post graduate student of General Medicine, Chengalpattu Medical College, Chengalpattu, under my guidance and supervision in fulfilment of regulations of The Tamilnadu Dr.M.G.R Medical University for the award of M.D. Degree during the Academic Period 2015 – 2018.
Prof. DR. R.NARMADHA LAKSHMI M.D, Dch, Department of General Medicine,
Chengalpattu Medical College, Chengalpattu.
Place:
Date:
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DECLARATION
I, Dr.A. RAJA, solemnly declare that the dissertation titled
“DEMOGRAPHIC, CLINICAL, INVESTIGATIONAL AND ETIOLOGICAL ROFILE OF PATIENTS WITH ACUTE SYMPTOMATIC SEIZURES” has been conducted by me during the period of October 2016 - September 2017 at Chengalpattu Medical College Hospital,under the guidance and supervision of Prof. Dr. R. Narmadha Lakshmi , M.D.,Dch.This dissertation is submitted to The Tamil Nadu Dr. M.G.R. Medical University, Chennai, in partial fulfilment of the regulations for the award of MD degree (branch I) General Medicine.
SIGNATURE OF THE CANDIDATE
Place:
Date:
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CERTIFICATE II
This is to certify that this dissertation work titled
“DEMOGRAPHIC, CLINICAL, INVESTIGATIONAL AND ETIOLOGICAL PROFILE OF PATIENTS WITH ACUTE SYMPTOMATIC SEIZURES” of the candidate Dr. A.RAJA with registration number 201511252 for the award of degree of M.D General Medicine ( Branch I ). I personally verified the urkund.com website for the purpose of plagiarism check. I found that the uploaded thesis file contains from introduction to conclusion and result shows 3 % of plagiarism in the dissertation.
Signature of the Guide
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ACKNOWLEDGEMENT
At the outset, I thank our Dean Dr. USHA SADASIVAN M.D,PhD, for permitting me to use the facilities of Chengalpattu Medical College and Government Hospital, Chengalpattu to conduct this study.
I wish to express my respect and sincere gratitude to my beloved teacher and Head of the Department of Medicine, PROF.Dr. V.R.MOHAN RAO, M.D., for his valuable guidance and encouragement throughout the study and also during my post graduate course. I owe my sincere thanks to him.
I also owe my sincere thanks to my beloved unit chief and my guide PROF.Dr.NARMADHA LAKSHMI M.D., for her guidance and support throughout the conduct of the study and also during my post graduate course.
I express my special thanks to Assistant Professor, Dr.Balaji M.D,DM (Neurology) for his valuable guidance. I am greatly indebted to my unit Assistant Professors, Dr.E.Arul Anandhan M.D., Dr.S.Sudha M.D., Dr.G.Gowthami M.D.
I also wish to express my respect and sincere gratitude to my beloved Professors Dr.Anusuya M.D., Dr.Manickam., Dr.Sheik Sulaiman Meeran M.D. I owe them a lot and sincerely thank them.
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I am extremely thankful to my Assistant Professors for their constant encouragement, timely help and critical suggestions throughout the study and also for making my stay in the unit both informative and pleasurable.
I also thank Assistant Professor, department of neurology , Dr.Hariharan ,M.D.,D.M., for extending his support during the period of study.
I also thank my Assistant Professors Dr.N.Ravishankar M.D., Dr.J.Chandru M.D., Dr.Jayalakshmi M.D., Dr.Senthilkumaran M.D. for their constant encouragement and help.
I profusely thank the Biochemistry, Radiology and Neurology Departments for their cooperation and support.
I extend my thanks to my family and my junior and senior postgraduates who stood by me during my times of need. Their help and support have been invaluable to the study. Finally, I thank all the patients, who form the most integral part of the work, were always kind and cooperative. I pray for their speedy recovery and place this study as a tribute to them.
CONTENTS
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S NO. CONTENTS PAGE NO
1. INTRODUCTION 1
2. REVIEW OF LITERATURE 4
3. AIMS AND OBJECTIVES 36
4. MATERIALS AND METHODS 38
5. RESULTS AND ANALYSIS 40
6. DISCUSSION 51
7. SUMMARY 60
8. CONCLUSION 61
9. BIBLIOGRAPHY 63
11. PROFORMA 70
12. MASTER CHART 79
LIST OF ABBREVIATIONS
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GTCS Generalised Tonic clonic Seizures EPC Epilepsia Partialis Continua
CT Computed Tomography
MRI Magnetic Resonance Imaging MRV Magnetic Resonance venography SAH Subarachnoid haemorrhage ICH Intracerebral Haemorrhage
TB Tuberculosis
ANA Anti Nuclear Antibody
dsDNA Double standard Deoxyribo Nucleic Acid
APLA Anti Phospholipid Antibody
CSOM Chronic Suppurative Otitis Media CVT Cerebral Venous Thrombosis
SSS Superior Sagittal Sinus LS Lateral Sinus
FND Focal neurological deficit HIV Human immunodeficiency virus
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NCC Neurocysticercosis RHD Rheumatic heart disease CAD Coronary artery disease CKD Chronic kidney disease HTN Hypertension
DM Diabetes mellitus
LVH Left ventricular hypertrophy AVM Arteriovenous malformations LFT Liver function test
ECG Electrocardiogram EEG Electroencephalogram CNS Central nervous system SCTEL Single CT enhancing lesion
SSCCCTL Small single cerebral calcific CT lesion
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INTRODUCTION
Acute symptomatic seizures are those caused or provoked by an acute medical or neurological insult, commonly seen in medical wards . Acute symptomatic seizure shows an clearly identifiable causal association, generally tend not to recur, and usually long term antiepileptic treatment is not needed. It can occur as a single event or brief clusters, focal with or without generalization , or generalized. Most common type is generalized tonic clonic seizures.
Status Epilepticus are usually seen in intensive care units. Focal seizures are usually associated with structural abnormalities of brain, but generalized seizures result from cellular, biochemical, structural abnormalities that have a wide spread distribution. In developing countries, CNS infections, metabolic disorders and cerebrovascular disorders predominate.
Seizures in the elderly are often due to cerebrovascular diseases like stroke, followed by metabolic and systemic disorders, traumatic brain injury, neoplasms, degenerative disorders, drug withdrawal, CNS infections.
The seizures can be associated with multiple factors in an individual, is best thought of an interaction between genetically determined seizure thresholds, underlying predisposing pathologies or metabolic derangements and acute precipitating factors.
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About 25 – 30% of first seizures are acute symptomatic seizures. The risk of recurrence is high in certain patients following these seizures (like in elderly). New onset acute symptomatic seizures can be a manifestation of acute neurological disorders.
The etiological spectrum and outcome of new onset acute symptomatic seizure may vary in developing countries from developed ones.
Approximately 60% of all epilepsies are idiopathic or cryptogenic. Numerous brain pathology can cause seizures. Cerebrovascular diseases are most commonly found among elderly. Status epilepticus presents as most common neurologic emergencies in children, adolescents, and young adults. Status epilepticus may be due to acute neurological conditions such as CNS infections or stroke, CNS tumors, head trauma, intractable epilepsy, metabolic disorders, drug withdrawal / overdose.
Data analysing the causes of acute symptomatic seizures, from south India are limited. So it is often useful to identify the various conditions producing seizures in our patients, using appropriate investigations to find out the underlying problem.
With the help of detailed clinical history, physical and neurological examination, analysis of blood and other body fluids, electroencephalographic (EEG) recordings, magnetic resonance imaging (MRI) and/or computerized tomography (CT) scans, the underlying cause of acute symptomatic seizures can be
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made out. An accurate diagnosis of the cause of acute symptomatic seizure is essential for the treatment as well as prognosis .The treatment of underlying cause will abolish the seizures in specific condition.
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REVIEW OF LITERATURE
A seizure is a paroxysmal event due to abnormal, excessive, or synchronous neuronal activity in the brain. Depending on the distribution of discharges, this abnormal brain activity can have various manifestations,ranging from dramatic convulsive activity to experiential phenomena not readily discernible by an observer. Although a variety of factors affect the incidence and prevalence of seizures , ~5-10% of the population will have at least one seizure, with the highest incidence occurring in early childhood and late adulthood.
Epilepsy describes a person with recurrent seizures due to a chronic, underlying process . This definition implies that a person with a single seizure, or recurrent seizures due to correctable or avoidable circumstances, does not necessarily have epilepsy. Epilepsy refers to a clinical phenomenon rather than a single disease entity . The various epilepsy syndromes present with the distinctive clinical and pathologic characteristics suggestive of a specific etiology.
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Seizures can be classified based on their supposed etiology, i.e., idiopathic (primary) or symptomatic (secondary), their site of origin; their clinical form (generalized or focal); their frequency (isolated, cyclic, or repetitive, or the closely spaced sequence of status epilepticus); or by special electrophysiologic correlates. The classification of seizure was first proposed by Gastaut in 1970 and was then refined repeatedly by the Commission on Classification and Terminology of the International League Against Epilepsy (1981), updated on 2005-2009.
This classification, based mainly on the clinical form of the seizure and its electroencephalographic (EEG) features, has been adopted worldwide and is generally referred to as the ‘International Classification’.
Definition :
Acute symptomatic seizure was defined as seizure caused or provoked by an acute medical or neurological insult. Acute symptomatic seizures were further grouped into two broad categories: 1) acute symptomatic seizure caused by acute neurological insult; and 2) acute symptomatic seizure caused by acute metabolic disorder.
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CLASSIFICATION OF SEIZURES ( ILAE 2005-2009)
1. Focal seizures
a. Focal seizures without dyscognitive features
b. Focal seizures with dyscognitive features
2. Generalized seizures
a. Absence (Typical , Atypical)
b. Tonic clonic
c. Clonic
d. Tonic
e. Atonic
f. Myoclonic
3. May be focal, generalized, or unclear Epileptic spasms
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Risk factors or etiology:
3.1 Symptomatic seizures or epilepsies - consequence of a known cerebral dysfunction
3.1.1 Acute symptomatic - seizures occur in close temporal association (within 7days) with an acute systemic, metabolic or toxic insult and with an acute CNS insult (infection, stroke, cranial trauma, intracerebral hemorrhage, acute alcohol intoxication or withdrawal).
3.1.2 Remote Symptomatic - seizures in relation to a well demonstrated antecedent condition called as remote symptomatic seizures or epilepsy (more than 7 days of cerebral insult).
3.2 Unknown etiology - no clear antecedent etiology can be detected .
The seizures are divided into two types – focal, in which a localized onset is possible & generalized, in which the seizures begin bilaterally. It is also useful clinically and etiologically to separate epilepsies that originate as truly generalized electrical discharges in the brain from those which spread secondarily from a focus.
The primary generalized epilepsies are a group of diverse, age-dependent phenotypes characterized by generalized, 2.5 to 4 Hz, bifrontally predominant spikes or
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polyspike-and-slow-wave discharges that arise without underlying structural abnormalities.
Seizures that begin locally and evolve into generalized tonic-clonic seizures, termed secondary generalized seizures, generally have no such genetic component and are usually the result of underlying brain disease, either acquired or due to congenital malformations or metabolic defects . Focal seizures vary with the site of the lesion, and are now divided into two groups, with or, without dyscognitive features, whether consciousness is retained or impaired. Focal seizures without dyscognitive features most often arise from a foci in the sensorimotor cortex. Focal seizures with dyscognitive features most often have their focus in the temporal lobe on one side or the other, but a frontal localization is also well known .
If the seizure lasts more than 15-30 minutes or persistent without recovery of consciousness it is called status epilepticus.
Epilepsia Partialis Continua is a type of focal motor epilepsy characterized by persistent rhythmic clonic movements of one muscle group—usually the face, arm, or leg—which will repeat at regular intervals every few seconds and may continue for hours, days, weeks, or months without involving other parts of the body. It is a highly restricted and persistent focal motor status epilepticus(2).
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The first solitary seizure or brief outburst of seizures may occur during the course of many medical illnesses, either the cerebral cortex has been affected by disease, primarily or secondarily. Status epilepticus especially generalized convulsive type indicate an medical emergency. A series of seizures may indicate ongoing neurological disease that demands the need for special diagnostic and therapeutic measures.
The age of the patient greatly affects the incidence of certain seizure types;
e.g., absence and myoclonic seizures are relatively more common in children and adolescents. The underlying cause varies greatly by age. In adolescence (12-18years), common causes are idiopathic epilepsy, including juvenile myoclonic epilepsy, trauma, CNS infections, brain tumors, drugs, congenital CNS abnormalities and in young adults (18-35 years), trauma, alcohol withdrawal, and illicit drug use. In older adults (over 35 years), cerebrovascular diseases, trauma (subdural hematoma), CNS tumors, degenerative diseases and metabolic disturbances are main causes.Strokes are most common in older age (over 65 years).
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HISTORY
History from a reliable attender is very important in the diagnosis of seizure. Type of seizure, risk factors, predisposing events, and past illness are essential to determine its pattern and other characteristics; and undertake a search for its cause. In the diagnosis of epilepsy, history and the physical examination are important to identify any underlying etiology .
PHYSICAL EXAMINATION
The general physical examination was done to look for signs of infection or systemic illness. Careful examination of the skin to look for markers of neurocutaneous disorders, such as tuberous sclerosis or neurofibromatosis, or chronic liver or renal disease. A finding of organomegaly may indicate a metabolic or storage disease, and limb asymmetry may provide a clue to brain injury early in development. Signs indicative of head trauma and use of alcohol or illicit drugs should be sought. Auscultation of the heart and carotid arteries are done to identify cardiovascular abnormalities.
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CNS EXAMINATION
All patients should undergo complete CNS examination, with particular emphasis on eliciting signs of cerebral hemispheric disease.
Abnormality in mental status (including memory, language function, and abstract thinking) may suggest lesions in the anterior frontal, parietal, or temporal lobes.
Visual field testing are done to look for lesions in the optic pathways and occipital lobes. Screening tests of motor function such as pronator drift, deep tendon reflexes, gait, and coordination may suggest lesions in motor (frontal) cortex, and cortical sensory testing (e.g. two point discrimination) may detect lesions in the parietal cortex.
LABORATORY STUDIES
Routine blood analysis are indicated to identify the more common metabolic causes of seizures, such as abnormalities in electrolytes, glucose, calcium, or magnesium, and hepatic or renal disease. A screen for toxins in blood and urine should also be obtained from all patients in appropriate risk groups, especially when no clear precipitating factor has been identified. A lumbar puncture is indicated in any case of suspected meningoencephalitis, and mandatory in all HIV patients, even in the absence of symptoms or signs suggesting infection.
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ELECTROPHYSIOLOGICAL STUDY
EEG should be done in all patients with possible seizure disorder. In a patient with suspected epilepsy, the presence of electrographic seizure activity during the clinically evident event clearly establishes the diagnosis. The absence of EEG seizure activity does not exclude a seizure disorder, however, because focal seizures arise from the area of cortex that is outside the range of the scalp electrodes.
Following GTCS, the EEG is always abnormal. Since seizures are usually infrequent and unpredictable, it is difficult to obtain the EEG during a clinical event.
Continuous monitoring for hospitalized patients using video-EEG telemetry units or the use of portable equipment to record the EEG continuously on cassettes for 24 hours in ambulatory patients has made it easier to monitor seizure activity effectively. The video-EEG telemetry is now utilized for the accurate diagnosis of epilepsy in patients with poorly characterized events or seizures that are difficult to control.
The EEG taken in the interictal period, shows epileptic form activity. The presence of epileptic form activity has greater prevalence in patients with epilepsy than in normal individuals. The initial routine interictal EEG may be normal even in the patients with epilepsy.
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EEG is helpful in classifying seizure disorders and the selection of anticonvulsant therapy. Focal interictal epileptic form discharges would support the diagnosis of a focal seizure disorder such as temporal lobe epilepsy or frontal lobe seizures, depending on the location of the discharges.
Also useful to assess the prognosis of seizure disorders; in general, a normal EEG implies a better prognosis, whereas an abnormal background or profuse epileptic form activity suggests a poor outlook.
The EEG has not proved to be useful in predicting epilepsy, in patients with predisposing conditions , such as head injury or brain tumor, since epileptic form activity is commonly present inspite of seizure activity.
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BRAIN IMAGING
Almost all patients with new-onset seizures should undergo brain imaging study to rule out any underlying structural abnormality.
MRI is better than CT to identify lesions such as tumors, vascular malformations, or other CNS pathologies that need immediate therapy.
The MRI fluid-attenuated inversion recovery (FLAIR), has increased the sensitivity for detecting abnormalities of cortical architecture, including hippocampal atrophy associated with mesial temporal sclerosis and also cortical neuronal migration. These findings may not indicate immediate therapy, provides an explanation for the patient's seizures and the need for chronic anticonvulsant therapy or possible surgical resection(11,12).
CT scanning should be performed urgently in cases of suspected CNS infection or mass lesion.
Functional imaging procedures such as positron emission tomography (PET) and single photon emission computed tomography (SPECT) are used in certain patients with medically refractory seizures.
Volumetric MR Imaging gives quantitative evaluation of hippocampal volume has been found to marginally increase the sensitivity over visual analysis in detection of hippocampal sclerosis. T2 Relaxometry
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is used to quantify the T2 signal in the hippocampus, in mesial temporal sclerosis, the relaxation time has proven to be lengthened by 10 milliseconds. MR Spectroscopy has been widely used in providing insight into the metabolic alterations in epilepsy (12).
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EPIDEMIOLOGY
Epidemiology of acute symptomatic seizure varies in different age groups and in different countries. In Developing countries, major cause is CNS infections. A study done at a university hospital in South India showed that seizures occur in close temporal association with an acute central nervous system (CNS) insult in 53% of patients. Cerebrovascular diseases were the risk factors for remote symptomatic seizures. Infections of CNS including single CT enhancing lesion (SCTEL) accounted for about 77% in patients with acute symptomatic seizures. SCTEL was defined as a disc or ring lesion less 20 mm and enhancing on contrast administration. Neurocysticercosis, SCTEL and small single cerebral calcific CT lesion (SSCCCTL) together accounted for 40% of etiological factors and CNS tuberculosis for 10%. Infections of the central nervous system and SCTEL together were the major risk factors in 52% of patients aged
≤40 years. The type of seizure was either focal with or without secondary generalization in 76% of patients.
Another study from south India (6) the etiological risk factors were central nervous system infections in 32% patients, metabolic disorders in 32%, cerebrovascular diseases (ischemic, venous and hemorrhagic) in 21% and others in 15%.
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The patients with CNS infections was meningoencephalitis in 43%
and parenchymal granuloma in 57% of patients, in that degenerative phase solitary cystic granuloma in 75% and tuberculoma in 25% of patients.
Study by Sander et al(13), the definite seizures were classified as cryptogenic in 62% (58-66%), remote symptomatic in 21% (18-25%), and acute symptomatic in 15% (12-18%). The aetiology of epilepsy was vascular disease in 15% (12-18%) and tumor in 6% (4-8%). Among older subjects the proportion with an identifiable cause was much higher; 49%
(41-58%) were due to vascular disease and 11% (6-16%) to tumor(13).
CEREBROVASCULAR DISEASES :
The most common cause among elderly is cerebrovascular diseases in developing countries. Cerebrovascular diseases may account for ~50%
of new cases of epilepsy in patients older than 65. Acute seizures i.e., occurring at the onset of stroke are more often due to embolic rather than hemorrhagic or thrombotic stroke. Chronic seizures typically appear months to years after the initial event and are associated with all forms of stroke.
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The reported incidence of post-stroke seizures varies widely between epidemiological studies, ranging from 2% to 33% for early seizures and 3% to 67%
for late seizures(5). According to Joseph et al, cerebrovascular disease is the most commonly identified cause of acquired epilepsy. Post-stroke seizures account for 11%
of all epilepsy, 22% of all cases of status epilepticus, and 55% of newly diagnosed seizures amongst older patients.
According to Maurizio et al, the risk of first seizure was increased in cortical involvement, multiple CT-scan lesions, supratentorial lesions, prior lesions on CT-scan, family history of seizures, use of epileptogenic drugs, large lesions, hemorrhagic lesions, and cortical atrophy.
Patients with CVT present with varying combinations of headache, seizures, aphasia, behavioral abnormalities, altered sensorium and focal deficits. Seizures may be focal, multi focal or generalized. The presentation is acute in obstetric and infectious CVT while a slowly progressive disease is more common in inflammatory and idiopathic cases. Thrombosis involves the dural sinuses as well as cortical veins producing cerebral infarction and neurological deficit .
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Seizures that begin in patients of adolescence and early adulthood may be associated with head trauma, CNS infections including parasitic infections such as cysticercosis, brain tumors, congenital CNS abnormalities, illicit drug use, or alcohol withdrawal.
HEAD INJURY :
Head trauma is a common cause of epilepsy in adolescents and adults.
A patient with a penetrating head wound, depressed skull fracture, intracranial haemorrhage, or prolonged post-traumatic coma or amnesia has a 40-50% risk of developing epilepsy, while a patient with a closed head injury and cerebral contusion has a 5-25% risk. Recurrent seizures usually develop within 1 year after head trauma, although intervals of 10 years are well known.
In controlled studies, mild head injury, defined as a concussion with amnesia or loss of consciousness of <30 min, was found to be associated with only a slightly increased likelihood of epilepsy.
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CNS INFECTIONS :
Infections are important cause of seizures in developing countries, the frequency of which may differ widely in different locations. Viral, bacterial, fungal and parasitic infections can result in seizures.
BACTERIAL MENINGITIS :
Bacterial meningitis of varying etiologies are often seen especially caused by pneumococci and even gram negative bacilli in immunocompromised individuals.
Tubercular meningoencephalitis can also manifest with seizures and other features like cranial nerve palsies.
VIRAL INFECTIONS :
Viral infection of the brain include either aseptic meningitis or encephalitis. The virus causing aseptic meningitis includes entero-virus(more common in developing countries because of faecal-oral transmission), mumps, arena viruses, herpes simplex type-2, varicella zoster and HIV(2).
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HERPES SIMPLEX ENCEPHALITIS :
Herpes simplex encephalitis has no pathognomonic clinical presentation but presents as focal encephalitis with malaise; focal seizures that may become generalized. Herpes simplex encephalitis produces dramatic electroencephalographic (EEG) focal, temporal or lateralized polymorphic delta activity as the earliest changes. CT and MRI reveal medial temporal lobe involvement.(14)
HIV INFECTION :
Seizures are common in patients with human immunodeficiency virus (HIV) infection, and this may be an important cause for acute symptomatic seizures. Seizures may rarely be the presenting compliant of HIV infection.
Opportunistic infections such as toxoplasmosis, tuberculosis, progressive multifocal leukoencephalopathy (PML), cryptococcal meningitis and polymicrobial infections, metabolic and electrolyte disturbances, and drugs are common causes of new-onset seizures in HIV. In the absence of any cause, primary HIV infection may be considered responsible for seizures .
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The treatment of HIV-infected individuals with seizures comprises of the administration of AEDs, specific treatment of the underlying conditions, and antiretroviral drugs.
NEUROCYSTICERCOSIS :
Neurocysticercosis is a disease caused by the infection with the larval stage of the intestinal cystode ( Taenia solium ) that occurs when humans become intermediate hosts. The parasite has marked tendency to infect muscle and the central nervous system where it produces a pleomorphic clinical disorder neurocysticercosis. In many developing countries, neurocysticercosis were the most common parasitic disease of the central nervous system and accounts for 10% of all acute neurological diseases.
There are wide variations of clinical manifestations of neurocysticercosis. These are consequence of inflammation around a cyst, space occupation and impedance to the flow of cerebrospinal fluid. Less commonly, there is meningeal or vascular inflammation.
Epilepsy is the most common manifestation of neurocysticercosis, occurring in two-third of affected patients.(3,4) Acute symptomatic seizures occur during the focal encephalitic illness caused by degenerating parasite but chronic
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epileptogenic focus that causes late epilepsy develops due to healing by perilesional gliosis and chronic calcified lesion. Seizures in neurocysticercosis are
generalized convulsive or simple focal with focal motor activity.
Medina et al. in their series of 50 patients with epilepsy due to neurocysticercosis found that 72% had focal seizures. Del Brutto et al. studied clinical characteristics of 203 patients with epilepsy and neurocysticercosis and found generalized convulsive seizures in 38% and focal seizures in 2%
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Neuroimaging is essential to the diagnosis of neurocysticercosis. Brain MRI is superior for showing intraventricular or subarachnoid cyst, and for showing inflammation around a cyst whereas CT is better for showing the calcified inactive lesions.
Recent MRI studies with gradient echo and reversed gradient echo phase image have shown scolex visible within the calcified lesion as visible on CT scan;
these entrapped antigens have been shown to be responsible for intermittent immunoallergic response, perilesional edema and seizure recurrence. There may be single or multiple cysts in different pathological stages(15).
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Carpio has proposed a classification system that corresponds to the viability of the parasite: active, transitional and inactive. Both CT and MRI can show the presence of the eccentric mural nodule (the invaginated scolex), an appearance when multiple is pathognomonic of neurocysticercosis (starry night appearance).
Magnetization transfer spin echo sequence of MRI and calculation of magnetization transfer ratios were used to differentiate neurocysticercosis from tuberculoma(16).
CEREBRAL MALARIA :
Malaria is the most common parasitic infection affecting CNS . Approximately 2% of all patients with malaria have cerebral involvement and nearly 80% of patients who ultimately die have cerebral involvement.
Cerebral malaria is fatal in 20% to 50% of affected patients. In countries like Nigeria where malaria is endemic, cerebral malaria is responsible for one third of seizures with fever in childhood.
TOXOPLASMOSIS :
In immune compromised patients, cerebral toxoplasmosis produces nonspecific signs and symptoms of intracranial mass lesion and seizures.
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In the developing world, toxoplasmosis may occur without HIV infection as well and linear beaded appearance on MRI may be diagnostic. Focal neurological deficits occurred in (69%) and seizure in (29%).
TUBERCULOMA OF BRAIN :
Brain tuberculomas appear as intracranial masses in about 5% patients in developing countries(17). Before effective chemotherapy was available for tuberculosis, tuberculoma made up 20 per cent of intracranial lesions in one large series(19). The incidence of neurotuberculosis in the United States is less than 0.5 per cent(18). Tuberculomas are granulomatous mass lesions made of a central zone of caseation surrounded by a collagenous tissue capsule arising in the brain parenchyma or the spinal cord. The commonest symptoms were headache (100%), focal or generalized seizures (68.7%) and hemiparesis with or without hemisensory symptoms (56.2%). The role of neuroimaging by CT or MRI scan in the diagnosis of tuberculoma is well established. MRI is superior to CT in visualizing the morphological details of tuberculoma, and particularly the ring enhancing tiny brain stem lesions. By using MR diffusion weighted imaging, spectroscopy and minimally invasive CT-guided biopsy, diagnostic efficacy can be improved.
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The few studies available from developing countries ,have shown complete radiological resolution of the intracranial lesions in 80-100% of patients on short-course (6-12 months) chemotherapy. A recent study from India, including only histopathologically verified cases, revealed a lower rate of 54% complete resolution by 24 months of treatment.
According to Jayasree et al 32% of cases of seizures were due to CNS infections, of this 4.5% contributed by tuberculoma.
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CEREBRAL ABSCESS:
Seizure is a common complication of cerebral abscess, frequently occurring at presentation. Early seizures predispose to late seizures and in these patients long- term anticonvulsant treatment should be considered. There is no relationship between the site of the abscess, organism cultured, surgical treatment, presumed aetiology, age or sex of the patient and seizure occurrence.
METABOLIC ETIOLOGY :
Metabolic disturbances such as electrolyte imbalance, hypo- or hyperglycemia, renal failure, and hepatic failure, hypernatremic
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hyperosmolar state, thyrotoxic storm, porphyria, hypomagnesemia, and hypocalcemia may cause seizures at any age.
Rapidly evolving electrolyte abnormalities are more likely to cause seizures than those occurring gradually. Similarly, endocrine disorders, hematologic disorders, vasculitides, and many other systemic diseases may cause seizures over a broad age range. A wide variety of medications ( like benzodiazepines and barbiturates) and abused substances are known to precipitate seizures.
HYPERGLYCEMIC STATES :
Both Diabetic ketoacidosis (DKA) and hyperosmolar coma can cause seizures. Hyperglycemic hyperosmolar state can manifest with features such as altered sensorium, focal motor seizures, transient hemiplegia, chorea, hemiballismus and hemichorea - hemiballismus.
RENAL FAILURE :
Patients with renal failure may manifest a variety of neurologic disorders.
Patients with chronic kidney disease who have not yet received dialysis therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremors, asterixis, multifocal myoclonus, and seizures.
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After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These CNS disorders are referred to as uremic encephalopathy.
The dialysis treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis dysequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. A study on nine patients, aged 23 to 67 years, showed a remarkable sequence of EEG findings in progressive uremic encephalopathy. The initial characteristics suggested a disorder of subcortical gray matter, followed by involvement of cortical gray matter and finally white matter. Seizures indicated a grave prognosis(26) .
When seizures occur in the presence of uremia, it is necessary to rule out a number of complications other than uremia: electrolyte imbalance (water intoxication, hypocalcemia, hyponatremia, hypomagnesemia, aluminum encephalopathy ), drug intoxication, hypertensive encephalopathy, intracranial hemorrhage, subdural hematoma and Wernicke’s encephalopathy.
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HYPONATREMIC SEIZURES :
Aggravation of seizures due to hyponatremia was investigated in five patients with epilepsy & polydipsia-hyponatremia. They experienced marked increases in the frequency of their focal seizures with dyscognitive features with a decrease in the serum sodium to 118-127 mEq/L. In all cases, the serum sodium level returned to normal through restriction of fluids, and the clinical seizures were improved.
OPC POISONING :
Seizure can occur in organophosphorus poisoning, in about 22-25% in children and 2-3% in adults. Electrographic seizures are a feature of organophosphate anticholinesterase intoxication(33). Clinical studies of pesticide poisonings suggest that seizures are more common in children than in adults. Since flaccid paralysis, a characteristic sign of organophosphate poisoning, can mask convulsions, the most reliable indicator of seizures is the electroencephalogram.
Seizures can rapidly progress to status epilepticus, contributing to mortality and, in survivors, to neuronal damage and neurological impairment.
Anticonvulsant drugs can significantly reduce the lethal and toxic effects of these compounds. A benzodiazepine, usually diazepam, is the treatment now used
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for control of seizures. Glutamatergic excitotoxicity is most likely cause for seizures . Future prospects for better treatments include newer benzodiazepines, glutamate receptor antagonists, antimuscarinics with additional antiglutamatergic activity and adenosine receptor antagonists.
The illegal mixing of organophosphates and pyrethroids in marketed agricultural insecticides in developing countries causes combination of miosis, bradycardia, tachypnea, and unconsciousness and seizures. The occurrence of papillary dilation and seizures after a small-dose infusion of atropine (0.08 to 0.2 mg/kg in 1-3 h) raises the possibility of pyrethroid poisoning.
ALCOHOL WITHDRAWAL SEIZURES :
Alcohol withdrawal siezure is seen when an individual reduces or stops alcohol consumption after prolonged periods of excessive alcohol intake.
Approximately 23-33% of patients with significant alcohol withdrawal have alcohol withdrawal seizures ("rum fits").
Seizures are usually brief, generalized, tonic-clonic in nature, and without an aura. They occur in a cluster of 1-3 seizures with a short postictal period. Focal seizures are also common.
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The incidence peaks 24 hours after the most recent alcohol intake.
Most seizures typicallyterminate spontaneously or are easily controlled with benzodiazepines.
Status epilepticus may occur in 3% of alcohol withdrawal seizures and should prompt investigation for other causes, as people with alcoholism are prone to head injuries, chronic idiopathic epilepsy, and meningitis.
BRAIN TUMORS :
Seizures affect 50% of patients with primary and metastatic brain tumors.
Focal seizures are most common , followed by secondarily generalized, depending on histologic subtype, location, and tumor extent.
The underlying pathophysiologic mechanisms of tumor-associated seizures are poorly understood andinclude theories of altered peritumoral amino acids, regional metabolism, pH, neuronal or glial enzyme and protein expression, as
well as immunologic activity. A change in the distribution and function of N-methyl-d-aspartate subclass of glutamate receptors also has been suggested.
The often unpredictable responses to seizures after surgical tumor removal indicate that multiple factors are also involved. Studies are needed to elucidate more clearly the pathophysiologic mechanisms of tumor-related seizures and to identify and develop the optimal AEDs. Oligodendroglial brain tumors, 75%
patients presented with symptoms related to seizures.
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TREATMENT
The treatment of seizures of all types can be divided into - the use of antiepileptic drugs, the surgical excision of epileptic foci and other surgical measures, the removal of causative and precipitating factors, and the regulation of physical and mental activity. Antiepileptic drugs are chosen based on type of seizure and patient characteristics. Conventional or first line AEDs like phenytoin, valproate, carbamazepine, oxcarbazepine are started initially. Newer agents like lamotrigine, topiramate, zonisamide, levetiracetam, felbamate can also be tried.
SEIZURE TYPE FIRSTLINE SECONDLINE
Tonic-clonic Lamotrigine, Valproate Phenytoin, Carbamezapine Oxcarbazepine, Topiramate.
Focal Lamotrigine, Carbamazepine Valproate, Topiramate Phenytoin, Levetiracetam Typical Absence Valproate, Ethosuximide Lamotrigine, Clonazepam Atypical absence, Valproate, Lamotrigine Clonazepam, Felbamate Myoclonic & Atonic
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Treatment of underlying condition along with AED is very important in patients with acute symptomatic seizures. For seizures caused by metabolic and withdrawal states, anticonvulsant therapy is usually not needed as long as the underlying disturbance is corrected. Any patient with recurrent seizures of unknown etiology or a known cause that cannot be reversed, should be promptly treated with AEDs.
Starting therapy in a patient with a single seizure event is controversial.
Patients with structural brain lesions like tuberculoma, NCC or single enhancing lesion brain tumor, brain abscess or vascular malformation need AED until resolution of lesion and maintained on antiepileptic medication for at least 1 year, an attempt is made to withdraw medications only if the patient has been declared completely seizure-free. In cases of refractory seizures, benefit may be achieved by surgical removal of epileptogenic foci in brain.
Single seizure following stroke may not be treated, AED can be given if risk of recurrence exists. For patients with CVT, AED is usually recommended for one year. Gabapentin and lamotrigine are the first line drugs for post stroke seizures.
For brain tumors, AED should be given before and after surgery to prevent seizures. Safer AEDs in uremic patients are lamotrigine, valproate and phenytoin.
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Patients with tuberculoma or TB meningitis should be treated with 6 months course of ATT, extended for 9 -12 months in unresolved cases.
Corticosteroids (oral /parenteral) started early, reduces complications. For brain abscess, high dose parenteral antibiotics and surgical drainage are required.
Neurocysticercosis is treated with albendazole 15mg/kg /d in 2 doses for 8-28 days or, praziquantel 50mg/kg/d tds for 15-30 days. AEDs are usually discontinued after 1-2 years.
For patients with CVT, anticoagulants initially intravenous followed by oral therapy, antibiotics in cases of septic thrombophlebitis. Patients withtumor have to be treated surgically followed by radiotherapy or chemotherapy.
Generalized Convulsive Status Epilepticus should be treated promptly as it is associated with high mortality and cardiorespiratory dysfunction, hyperthermia, and metabolic derangements can occur as a result of prolonged seizures, which can lead to irreversible neuronal injury.
Rapidly assess cardiorespiratory function, airway and insert large- bore intravenous line and draw blood for glucose, blood urea nitrogen, electrolytes, and a metabolic and drug screen. A normal saline infusion is begun and a bolus of glucose is given (with thiamine if malnutrition and alcoholism are factors).
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Diazepam is given intravenously at a rate of about 2 mg/min until the seizures stop or a total of 20 mg has been given or lorazepam, 0.1 mg/kg given by intravenous push at a rate not to exceed 2 mg/min. A loading dose 20 mg/kg of phenytoin is administered by iv at a rate of less than 50 mg/min or fosphenytoin at 150 mg/min.
If the seizure is not controlled, repeat phenytoin 7-10mg/kg. Alternatives like sodium valproate 25mg/kg or phenobarbitone 20mg/kg infusion can be tried. If the seizure still continues, admit in ICU and give iv anaesthesia with midazolam or propofol as next step. Once the seizure is controlled, maintenance AED continued.
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AIMS AND OBJECTIVES
The aims of the study were as follows :
1. To analyze the etiological factors in patients>12 years of age presenting with acute symptomatic seizures .
2. To study the incidence of potentially curable causes of seizures.
3. To study the pattern of seizures and associated features.
4. To study the usefulness of various investigations in the diagnosis of acute symptomatic seizures.
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MATERIALS AND METHODS The Study Group:
The study was conducted on patientsadmitted in medical wards and IMCU of Chengalpattu Medical College Hospital, Chengalpattu.
Approval from the hospital ethical committee was obtained.
Study Design:
The study was a cross sectional study conducted for a period of one year between October 2016 -September 2017.
Inclusion criteria:
1. Patients admitted with first episode of seizure . 2. Age more than 12 years.
3. Patients admitted for other medical conditions who develop seizure during hospital stay.
Exclusion criteria
1. Excludes all patients under 12 years of age.
2. Hyperventilation, TIA, psychogenic seizures, movement disorders (choreoathetosis, tic disorder)
3. Patients with known epilepsy disorder taking antiepileptic drugs.
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METHODS
Consecutive patients with new-onset acute symptomatic seizure as the first presenting event with acute illness admitted in medical wards and IMCU of Government Hospital, Chengalpattu were studied. A total number of 285 patients were studied, out of which 200 were included in the study as per inclusion and exclusion criteria.
All details were noted in a proforma, a copy of which is annexed.
All patients were from low socioeconomic status. A detailed history was recorded from the relatives about the details of seizure event and, associated symptoms like fever, headache, vomiting, weakness or loss of consciousness.
Past history of medical or neurological illness was noted. Complete neurological examination was made to find out any etiological factors, focal neurological deficits or complications. Fundus examination was done to look for papilledema, or retinopathy.
Blood pressure values were recorded and categorised to different stages as per JNC 8.
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Baseline investigations done to find out metabolic changes, renal and liver function, electrolyte imbalances. ECG was done for all patients to exclude cardiovascular abnormality. CSF analysis done for indicated patients. CT brain was done for all patients with seizures as an neurological emergency. MRI brain was done only when CT is normal or doubtful diagnosis like brain tumours, and for imaging of sinuses and venous system . CT or MR angiogram was done for patients with CVT, AVM or other vascular abnormalities . Special MRI sequences like FLAIR, DWI, MR spectroscopy were done to differentiate between different lesions. Patients were treated according to type of seizure and underlying etiology. EEG done routinely for all patients in the interictal period.
All patients details were recorded using a master chart and statistical analysis done using epidemiological tools. The range, mean, and standard deviation were all calculated and results are analysed depending on the age group, causes and investigations used for the study. The outcome of the study can be finally made out.
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RESULTS AND ANALYSIS
Majority of the patients were from in and around Chengalpattu. Age of patients varied from 12 to 85. Majority of patients were from low socioeconomic class. Age distribution of patients is given in table 1.
Table 1: Age Distribution
AGE GROUP CASES
NO %
12 - 20 years 36 18
21-40 69 34.5
40-60 62 31
>60 33 16.5
Total 200 100
Range Mean S.D.
12 – 85
\ 38.5 17.4
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Table 2: Sex Distribution
Sex CASES
NO %
MALE 106 53
FEMALE 94 47
TOTAL 200 100
Among 200 patients 106 were males and 53 are females.
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Table 3:Typeof Seizures
Type of Seizures CASES
NO %
Focal 28 14
Focal Generalised 40 20
GTCS 122 61
EPC 10 5
TOTAL 200 100
Among 200 cases 28 patients presented with focal seizures, 40 with focal seizure with secondary generalization and 122 with GTCS. 10 were presented with epilepsia partialis continua. Out of these 200 cases, 10 had Status epilepticus. Most common presentation was generalised tonic clonic siezures, when compared GTCS are common in middle age.
Table 4 : Associated Symptoms
Symptoms Present Absent
No % No %
Fever 75 37.5 125 62.5
Headache 75 37.5 125 62.5
Vomiting 75 37.5 125 62.5
CSOM 4 2 196 98
Trauma 6 3 194 97
Weakness of Limbs
40 20 160 80
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Patients with acute symptomatic seizures due to infections and CVT had headache, vomiting and fever. 75 patients had fever at the time of seizures. Patients with meningitis, brain abscess, encephalitis were presented with fever . Patients who had mass lesions like tumor, neurocysticercosis, tuberculoma or abscess and CVT are presented with headache and vomiting.
Table 5 : Past Illness
Past Illness CASES
NO %
None 120 60
DM 24 12
HTN 24 12
Tuberculosis 6 3
Meningitis 8 4
Malignancy 4 2
HIV positive 4 2
Cardiac problem 6 3
CKD 10 5
Among these 200 patients 24 are diabetic, 24 were hypertensive, 6 had tuberculosis, 8 had past history of meningitis, 4 had malignancy of breast and lung. 4 were HIV positive.
6 patients had cardiac problem and 10 had CKD.
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Table 6 : Altered Sensorium
Altered Sensorium CASES
NO %
Absent 30 15
Drowsy 135 65
Stupor/ Coma 40 20
Total 200 100
Normal level of consciousness was present only for 30patients .There is change in level of consciousness. Among 200 patients 135 are drowsy and 40 patients were in stupor or coma. Fundus examination was normal in 134 patients and there was papilledema for 40 cases and 16 cases had retinopathy due to diabetes, hypertension related. Blood pressure was high in 68 patients.
Table 7: Focal Neurological Deficit Focal Neurological
Deficit
CASES
NO %
Absent 134 67
Right Hemiplegia 8 4
Left Hemiplegia 30 15
Monoplegia- Right 10 5
Monoplegia-Left 8 4
Homonymous hemianopia
4 2
Cranial nerve palsy 6 3
Total 200 100
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Among 200 patients with acute symptomatic seizures, 66 patients had focal neurological deficit . 38 patients present with hemiplegia, monoplegia was there for 18. Hemianopia and cranial nerve palsy was present for 10 patients. All these patients weakness persisted during hospital stay .
All baseline investigations done for all patients. Out of 200 cases, 12 patients had hyperglycemia and 4 had hypoglycemia. On adequate glycemic control, seizures were controlled .There were 10 patients with elevated urea and creatinine. All these patients had features of uremia and seizure controlled with AED followed by dialysis. Out of 200 cases, 6 patients had hyponatremia with Na values <120meq/l. Among these 6 patients, 3 had other associated metabolic abnormalities and in 3 patients, seizure was purely due to hyponatremia .
LFT was abnormal in 28 patients. Chest X-ray was abnormal in 18 patients. Out of 18 pateints, 4 had mass lesion, 4 had tuberculosis and 10 had cardiomegaly. ECG was normal in patients, left ventricular hypertrophy was there for 14 patients, features of coronary artery disease was there for 3 patients and 1 patient had arrhythmia.
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Table 8: EEG
EEG CASES
NO %
Normal 120 60
Diffuse slowing 20 10
Focal spikes and sharp waves
36 18
Bilateral spikes 24 12
Total 200 100
EEG was normal in 120 cases out of 200. Among 80 abnormal cases, 20 showed diffuse slowing, 36 cases showed focal spikes and sharp waves and 24 showed bilateral spikes and waves.
Table 9: Underlying cause and CT Scan findings
CT scan findings
% of Underlying Cause
Infection Metabolic CVT Stroke Tumour Calcified Graunuloma
Others
Normal 10 100 12 10 - - 30
Abnormal 90 - 88 90 100 100 70
57 0
5 10 15 20 25 30 35 40
Underlying cause
Underlying cause
Table 10: Underlying cause
Underlying cause CASES
No %
Infection 56 28
Metabolic 76 38
Stroke 24 12
CVT 10 5
Calcified granuloma 18 9
Tumor 6 3
Others 10 5
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Table 11 : Underlying cause and Age
Infections were most common cause among patients below 20 years of age. Adults aged 20-30 years, infection was most common followed by CVT and metabolic. In patients with 30-40 age group, most common cause was metabolic followed by infection. Patients aged 41-60, most common etiology was metabolic abnormalities and next common was stroke and infections. Patients >60 years metabolic causes were leading followed by stroke and tumors.
Infections were common in younger patients, metabolic abnormalities were the common causes in adults and elderly. CVT and single calcified lesion was common in 20-30 years of age. Stroke and tumors common in patients >50 years of age.
Age group
% Underlying cause
Infection Metabolic Stroke CVT Tumor Calcified granuloma
Others Upto20
years
68.3 12.7 4.6 1.4 3 10
21-30 years
35.2 22.8 3.4 29.6 - 3 6
31-40 30 48.4 6.6 9.8 - - 5.2
41-50 31.3 41.7 7 8 7.7 2 2.3
51-60 28.1 49.9 12.3 4 1 2.7 2
>60 2 55.5 24.5 - 10 5 3
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METABOLIC – MOST COMMON CAUSE
DIAGNOSIS FREQUENCY PERCENT
Alcohol associated 24 31.5
Hyperglycemia/hypoglycemia 12+4 21
Electrolyte disturbances 10 13
CKD 10 13
Hepatic encephalopathy 6 8.5
OPC 4 5
Drugs / Toxins 6 8.5
Total 76 100
Among metabolic causes 24 patients presented with alcohol withdrawal/ intoxication induced seizures, hyperglycemia associated seizures in 12 patients, hypoglycemia were 4 patients. Electrolyte disturbances in 10 patients, that includes hyponatremia, hypocalcemia.
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Uremia induced seizures in 10 patients, hepatic encephalopathy in 6 patients, drug induced seizures includes 6 patients, organophosphates poisoning in 4 patients.
INFECTION - SECOND MOST COMMON CAUSE
DIAGNOSIS FREQUENCY PERCENT
Bacterial meningitis 10 18
Tubercular meningitis 22 39.5
Neurocysticercosis 4 7
Encephalitis 10 18
Brain abscess 4 7
Brain abscess with CVT 2 3.5
Osteomyelitis, Epidural abscess, cerebritis
4 7
Total 56 100
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DISCUSSION
Government Hospital, Chengalpattu is the only tertiary referral care hospital located in Kanchipuram district. Various cases have been referred from Government sector hospitals like PHCs, Taluk hospitals, District head quarters hospitals, and many private hospital of not only from Chengalpattu but also from near by districts. Study of acute symptomatic seizure patients from October 2016 to September 2017 included 200 patients.
DEMOGRAPHY
Acute symptomatic seizure is an important cause of morbidity in our part of the country. It is very important to find out the underlying cause and its treatment for prevention of recurrent seizure. Acute symptomatic seizure is different from epileptic syndromes as it is curable by treating the underlying cause. Even if AEDs are used to suppress recurrence of seizures, they generally do not need to be continued after the patient has recovered from the primary illness. These concepts are based on the basic assumption that acute symptomatic seizures presumably cease with the resolution of the precipitating cause or illness. But seizure can recur in conditions like tumor ,stroke and head injury .
Among our 200 patients, 106 cases were males and 94 cases of females in our study. The mean age is 38.5 and there is patients from 12 to 85 years of age. Study by Sander et al (13) the proportions of males and females were similar. Usha Kant
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Misra et al ‘s study the median age of the patients was 37 years from 16-78 years.
According to Jaishree T Narayanan et al the mean age of patients with acute symptomatic seizures was 49.07 + 20.29 years (six months to 80years) as they had included pediatric patients in their study. In our study, less than 20 years were 18% , 21-40years of age were 34.5 % , 41-60 years 31 % and more than 60 years were 16.5 %. Younger adults are major category in our study group. Study by Sander et al 25% (21-28%) were younger than 15 years and 24% (21-28%) were 60 years or older. Twenty-four (36%) were aged 60 years and above in Jaishree T Narayanan et al study .
MODE OF PRESENTATION
In our study 61% of patients the type of seizure is GTCS and 20% focal with secondary generalization and14% presented with focal seizure and 5% with epilepsia partialis continua . Our study correlates with previous studies. Study by Usha Kant Mishra et al, generalized tonic-clonic seizure was the seizure type in 36 (55%) patients and in the remaining 30 (45%) patients, the seizure type was focal with or without secondary generalization. Of the 30 patients with focal seizures, 28 (93%) had complex partial seizure and two( 7%) had epilepsia partialis continua in their study .According to Sridharan et al in the new cases of epilepsy 50% have seizures of focal origin and 50% of generalized origin before the age of 40 years. After 40 years, the proportion of partial
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epilepsy rises to 75% by the age of 75. Study by Clifford Scholda total of 56%
of the patients had focal motor seizures, and in 44%, the seizures were generalized. Study by J. M. K. Murthy & Ravi Yangala type of seizure was simple focal or complex focal with or without secondary generalization in 412 (78%) patients and either unlocalized or generalized in 114 (22%) patients..
ETIOLOGY
Most common cause of seizure in our study is metabolic followed by infection and vascular insult to brain. 38 % patients had seizure due to metabolic insults. Out of 200 cases 38% of cases are due to metabolic and toxic, 28% due to infection, 12% due to stroke, 3% due to tumor, 5% due to CVT and 9% are due to single calcified lesions. 5% are classified as others include arachnoid cyst, AVM, Alzheimer’s disease.
In our study, 38% are due to metabolic and toxic causes. Jaishree T Narayanan et al study showed metabolic disorders in 32% of cases of seizures . In our study, there are 24 cases are due to either alcohol withdrawal /intoxication, hyperglycemia 12 cases and hypoglycemia 4 cases, electrolyte disturbances include hyponatremia, hypocalcemia about 10 cases, 10 cases of uremia, 6 cases are due to hepatic encephalopathy, OPC poisoning 4 cases, drug and other toxin 6 cases. Study by Jaishree T Narayanan (6) out of 21 cases, 15 were due to hyponatremia, 4 were due to hyperglycemia, 2 were due to hypoglycemia . In our study, 6 cases of seizures, 2 were related to toxins, out of that, 2 were due to organophosphorus poisoning, another 2 cases cypermethrin poisoning and 2 cases were tricyclic antidepressant
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overdosage. Study by Jaishree T Narayanan (6) there was 6 cases of alcohol related seizures and 2 cases of hypoxic encephalopathy .
In our study 28% are due to infection and calcified granuloma single or multiple 9%. Another study from south India by Jaishree T Narayanan (6) showed central nervous system (CNS) infections in 32% patients. Study by J. M. K.
Murthy et al seizure occurred in close temporal association with an acute central nervous system (CNS) insult in 53% of patients. Infections of CNS including single CT enhancing lesion accounted for 77% of patients with acute symptomatic epilepsy. Study by Ravindra Kumar Garg et al(23) infective pathologies were the most common etiology.
In our study out of 56 cases of infections, 22 (39.5%) cases are due to tubercular meningitis, 10 (18%) are due to bacterial meningitis, 10 (18%) cases are due to encephalitis, 4 (7%) cases are due to neurocystcercosis, 4 (7%) case due to osteomyelitis, epidural abscess, 4 (7%) case are due to brain abscess. The distribution of the pathology according to Jaishree T Narayanan et al (6) in patients with CNS infections was meningoencephalitis in 43% and parenchymal granuloma in 57% of patients out of that 75% due to degenerative phase solitary cystic granuloma and 25% due to tuberculoma.
Study by J. M. K. Murthy et al Neurocysticercosis, SCTEL and small single cerebral calcific CT lesion (SSCCCTL) together accounted for 40% of etiological factors and neurotuberculosis for 10%.
