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Organic Brain Disorders
Vinnci Angelica G. Dela CruzBS Psychology IIISeptember 30, 2014
Why organic?
Organic due to :
• Primary Brain Pathology
• Secondary Brain Dysfunction to Systemic Disease
Suspicion of organic mental disorder : 1. First Episode 2. Sudden Onset 3. Older Age at onset 4. Hx of Drug/Alcohol abuse 5. Concurrent
medical/neurological problem 6. Neurological signs: Seizures, LOC, Head injury, sensory motor deficit. 7. Presence of Confusion/Disorientation 8. Presence of visual
and non auditory (olfactory, gustatory, tactile) hallucinations
Definition• Abnormal cognitive state
– Defining feature = confusion
• Global cognitive impairment– Disordered behaviour– Emotions– judgment– Language– Abstract thinking– Psychomotor activity
• Lots of underlying disorders– CNS disease– Systemic disorders– Toxicologic
Definition
• Acute Organic Brain Syndrome– Delirium
• Chronic Organic Brain Syndrome– Dementia
Part of Brain Affected
• Brain damage affects the brain cortex or upper layer
• Cause problem with memory, language, thinking & social behaviour
• Eg: Alzheimer’s & Creutzfeld –Jakob disease
cortical
• Affects brain below the cortex
• Changes in emotion & movement
• Eg Huntington’s disease, Parkinson’s disease & AIDS
subcortical
Etiology
• Alzheimer’s disease
• Parkinson disease• Lewy body dementiaDegenerative
• Pseudodementia of depression
• Cognitive decline in late life scizophreniaPsychiatric
• Multi infarct dementiaVascular
• multiple sclerosis Demyelinating
• Vitamin def (e.g vit B12,folate), endocrinopathies (eg hypothyroidism), abnormality of cortisol metabolism
Metabolic
Etiology
• Prion disease ( Creutzfeld –Jakob disease)• AIDSInfection
• Alcohol, heavy metals, irradition, pseudodementia d2 medication (anticholinergics), carbon monoxide
Drugs and toxins
• Huntington disease, trauma(dementia pugilistica in boxers), tumorOthers
A. DELIRIUM
• Commonest organic mental disorder• Definition: Acute organic brain syndrome
characterized by clouding of consciousness and disorientation develops over a brief period and remits immediately once offending cause is removed.
• Epidemiology: - 5 to 15% of medical & surgical px; - High in post op patients; - 40-50% recovering from hip surgery; - Highest rate in post cardiotomy patients; - 30% in ICU
Clinical Features
1. Acute
2. Clouding of conciousness
3. Disorientation (mostly time, severe cases place and person)
4. Short attention span/distractibility
5. Perceptual Distortion
6. Disturbance in sleep wake cycle
DECREASE AWARENESS TO SURROUNDING
DECREASE ABILITY TO RESPOND TO ENVIRONMENTAL STIMULI
ILLUSIONSHALLUCINATIONS Mostly Visual
INSOMNIADAY TIME SLEEPINESS
7. Sun Downing – six in evening8. New Memory Impairement Relatively intact remote memory
9. Speech
10.Mood – Fear, anger rage
11.Delusions – Fleeting and fragmentary
12.Neuro: Tremors, Dysphasia, Urinary incontinence
IMPAIRED IMMEDIATE RECALL
IMPAIRED RECENT MEMORYSLURRING of SPEECHINCOHERANCE
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Predisposing Factors
• Old age
• Pre existing brain damage/dementia
• Past history of delirium
• Alcohol /drug dependence
• Chronic Medical illness
• Surgical procedures
• History of Head Injury
Organic ETIOLOGY of DeliriumCLASS ETIOLOGY
METABOLIC Hypoxia, Anemia, Electrolyte disturbance, Hepatic&Uremic Encephalopathy, Cardiac failure,arrest,arrythmia, Hypoglycemia, Metabolic acidosis&alkalosis, Shock
ENDOCRINAL Pituitary, Thyroid, Parathyroid, Adrenal dysfunctions
DRUG/SUBSTANCE
(Many) including alcohol, benzodiazepines, anticholinergics, psychotropics, lithium, AntiHPT, diuretics, anticonvulsant, digoxin, heavy metals, Insulin, salicylates
NUTRITIONAL DEFICIENCIES
Thiamine, Niacine, Pyridoxine, Folic Acid
INFECTIONS (ACUTE/CHRONIC) Septicemia, Pneumonia, Endocarditis, UTI, Meningitis, Encephalitis, Cellulitis
INTRACRANIAL Stroke, Post Ictal, Head Injury, Infections, Migraine, Focal abscess/neoplasms, Hypertensive Encephelopathy
MISCELLANEOUS Post op, ICU, Sleep deprivation
Management of Delirium
• If cause not known – Do a battery of investigations : CBC, Urinalysis, Blood glucose, Blood urea serum analysis, Liver and renal function test, arterial p02, Pco2, Thyroid function, B12, Folate levels, CSF, ECG, Drug screen,HIV, EEG, CT & MRI
• Correct underlying cause – • If underlying cause is found then it must be treated
immediately . For ex– 50mg of 50% IV dextrose for HYPOGLYCEMIA– 02 for HYPOXIA– IV fluids for electrolyte imbalance
• Drugs given if patient is agitated (most are):–Small dose
BENZODIAZEPINES (Lorazepam, Diazepam)
–ANTIPSYCHOTIC (Haloperidol)
MAINTAIN WITH ORAL HALOPERIDOL, LORAZEPAM TILL RECOVERY IN 1 WEEK
REVIEW DOSE, TAPER AND STOP
DELIRIUM VS DEMENTIA
B. DEMENTIA
• Definition: Chronic Mental Disorder characterized by impairment of intellectual functions, Impairment of memory and deterioration of personality with the course being progressive, stationary or reversible
CLINICAL FEATURES
• Duration: 6 months
• Impaired Intellectual functions
• Impairement of memory (initially mild, remote memory in later stage)
• Deterioration of personality with lack of personal care
• No conscious impairment
• Orientation-usually normal but falls later
• Aphasia – Difficulty in naming an object• Hallucinations and Delusions
• Additional:-
- Emotional lability: Marked variable emotional expression
- Catastrophic rxn: When asked to do something beyond her intellectual capibility, she goes into a rage
Types and causes Of DementiaTYPE CAUSES
Parenchymatous Brain Disease
Alzheimers Disease, Parkinson’s disease, Huntingtons’s Chorea, Pick’s Disease, Steel-Richardson syndrome (prog. Supranuclr palsy)
Vascular Dementia
Multiinfarct Dementia, Subcortical Vascular dementia (Binswanger’s disease)
Toxic Dementia
Alcohol, Drugs, Heavy Metals, Bromide, CO, Benzodiazepines, Psychotropics
Metabolic Dementia
Chronic hepatic/uremic encephalopathy, dialysis dementia, Wilson’s disease
Endocrinal Pituitary, Parathyrois, Thyroid, Adrenal dysfunction
Deficiency Dementia
Pernicious anemia, Pellagra, Folic acid, Thiamine deficiency
Infections AIDS, Neurosyphillis, Chronic Meningitis, Creutzfelft-Jacob disease
IOP ↑ Brain tumor, Headinjury hematoma, hydrocephalus Commonest: ALZHEIMERS DEMENTIA, MULTIINFARCT DEMENTIA, HYPOTHYROID
DEMENTIA, AIDS DEMENTIA COMPLEX
MANAGEMENT OF DEMENTIA
• Basic investigations
• Treat underlying cause – mentioned
• Symptomatic management of anxiety, depression, Psychotic symptoms
• Education – Family, Financial, Support groups
• Institutionalize in later stage
MANAGEMENT OF DEMENTIA
Non- pharmacological
Pharmacological Caregivers InterventionCognition Behaviour Mood
Promoting independence: communication, ADL skill training, exercise, rehabilitation, combination
Maintainence of cognition: reality therapy, Validation, life review
Cholinesterase inhibitors: donepezil•Mild, moderate and severe AD•Vascular dementia•Dementia with Lewy Body (DLB)
Atypical antipsycotics:
•can be used agitation and psychosis•Avoid in DLB
Antidepressants Evaluate caregiver needs
Multicomponent intervention:•Psychotherapy•Psychoeducation•Supportive therapy•Respite/day care•training
Alzheimer disease• First described by Alois Alzheimer in 1907• Although cause remains unknown, progress had been made to try
to understand molecular basic of amyloid deposits • genetic factors
–a minority (<7%) of AD cases are familial, autosomal dominant–3 major genes for autosomal dominant AD have been identified:•amyloid precursor protein (chromosome 21)•presenilin 1 (chromosome 14)•presenilin 2 (chromosome 1)–the E4 polymorphism of apolipoprotein E is a susceptibility genotype (E2
is protective• Biochemical factors
–Neurotransmitter such as Ach and Norepinephrine become hypoactive–Neuroactive peptides somatostatin and corticotrophin also decreased in concentration
DSM-IV-TR diagnostic criteria for dementia of Alzheimer’s type
• A. Development of multiple cognitive deficits manifested by both:
–1) memory impairment–2) ≥1 of the following cognitive disturbances:•Aphasia•Apraxia•Agnosia •Disturbances in executive functioning
• B. cognitive deficits in criteria A1 and A2 cause significant impairment in social and occupational functioning and represent a significant decline from a previous level of functioning
• C. gradual onset and continuing cognitive decline• D. not due to any other
–CNS conditions–Systemic conditions–Subtance-induced conditions
• E. Deficits do not occur during the course of delirium
• F. Disturbance is not better accounted by other Axis-I disorder (MDD, Schizophrenia)
Risk factors
• Aging (elderly people > 65 years of age)• Female• Family history
-Defective genes on chromosomes 1,14,21• Hypothethical risk factor : aluminium toxicity• Having history of head injury• Low education level • Smoking• Down syndrome
Pathology • Macroscopic appearance of brain : diffuse
atrophy, esp frontal, parietal and temporal lobes, flattened sulci & enlarged cerebral ventricles
• Microscopic findings : senile plaques (amyloid plaques – amount indicates severity), neurofibrillary tangles (composed of cytoplasmic skeleton, mainly phosphorylated tau protein), neuronal loss(in cortex & hippocampus), synaptic loss ( 50 % in cortex) & granulovascular degeneration of neurons
Course, prognosis & treatment
• Slowly progress memory impairment• Aphasia, apraxia and agnosia also present• May later develop motor & gait disturbances;
may become bedridden• Mean survival is 7 years from onset• Treatment : cholinesterase inhibitor (eg:
galantamine, rivastigmine, donepezil)
• There is a new case of dementia every 7 seconds in our world
• Alzheimer is the most common cause of dementia and is not part of aging process
• There are currently no prevention and cure for it
Vascular dementia• Caused by blockage of in brain’s blood supply• Leading to progressive decline in memory & cognitive
functioning• ♂> ,affects people between the ages of 60 and ♀
75, HTN or CV dss• Approximately 10-15% have coexisting vascular
dementia and dementia of Alzheimer’s type • Pathology : a/w multiple infarcts coz by
thromboembolism fr extracranial arteries arteriosclerosis in main vessels
Vascular dementia• Clinical features:
-sx are fluctuating & episodes of confusion are common esp at night-Neurological signs is common-in some cases emotional & personality changes may be apparent b4 impairment of memory & intelect
• Diagnosis, other signs and symptoms are as according to DSM-IV diagnostic criteria
• Prognosis -lifespan averages is 4-5 years from time of diagnosis
C. ORGANIC AMNESTIC SYNDROME
• Characterized by– Memory impairment (anterograde, retrograde
amnesia) due to an underlying organic cause.– No impairment of global intellectual function,abstract
thinking,personality.• Caused by Thiamine deficiency in alcohol dependence
as part of Wernicke Korsakoff Syndrome• Any other lesions involving bilaterally the inner core of
limbic system(i.e mammillary bodies,fornix,hippocampus, medial temporal lobe)
• The Lesions include:
• Head trauma
• Surgical procedure
• Hypoxia
• Posterior cerebral artery stroke
• Herpes simplex encephalitis
Management
• Treat the underlying cause if treatable.Ususally treatment is of not much help,except in prevention of further deterioration and the prognosis is poor
D. Other Organic Mental Disorders
• Organic Hallucinosis
• Organic Catatonic Disorder
• Organic Delusional (Schizo like) disorder
• Organic Personality Disorder
Organic Hallucinosis
• Etiology:
• Drugs:Hallucinogens,cocaine,cannabis,bromide)
• Alcohol:In alcoholic hallucinosis,auditory hallucinations are more common
• Migraine
• Epilepsy: Complex partial seizures
• Brain stem lesions
• Persistant or recurrent hallucinations due to an underlying organic cause.
• No major disruption of consciousness, intelligence or memory
Management 1)Treatment of the underlying cause if
treatable. 2) Symptomatic treatment with a low dose
of an anti-psychotic drug.
Organic Catatonic Disorder
• Etiology:• Neurologic disorders: limbic encephalitis,Surgical
procedures,sub dural hematoma,cerebral malaria• Systemic and metabolic disorders : Diabetic ketoacidosis
, pellagra, SLE, Hepatic encephalopathy• Drugs and poisoning: Organic alkoloids ,aspirin,lithium
poisoning ,ethyl alcohol , co
• Psychiatric disorders : manic stupor , periodic catatonia , reactive psychosis ,schizophrenia
Management
• Treatment of underlying cause
• Symptomatic treatment with low doses of benzodiazipam or an anti-psychotic or electro convulsive therapy.
Organic delusional disorder
• Predominant delusions which are persistant or recurrent ,caused by an underlying organic cause.
• No major disturbance of consciousness,orientation , memory or mood.
• Etiology:• Drugs:Amphetamines,cannabis,disulfimes• Spino cerebellar degeneration • Complex partial seizures
Management
• Treatment of underlying cause
• Symptomatic treatment with low doses of benzodiazipam or an anti-psychotic or electro convulsive therapy.
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CONVULSIVE DISORDES
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OVERVIEW
Convulsive phenomena are among the most frequently observed neurological dysfunctions in children and can occur with a wide variety of conditions involving the C.N.S
3-5% of all children will have one or more seizures .
The incidence of epilepsy (new cases per year) has been reported to be 50/100,000
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Etiology of Seizures in Children
classification of seizures is presented in the following : A) Acute/Non-recurrent
(i) with fever: febrile convulsion, infections e.g. meningitis, encephalitis. . (ii) without fever: poisoning including medicinal overdose, metabolic disturbance e.g. hypoglycemia, hypocalcaemia and electrolyte imbalance, head injury, brain tumor.
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Etiology of Seizures in Children
B) Chronic/Recurrent : (i) with fever: recurrent febrile convulsion. (ii) without fever: epilepsy.
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Febrile seizures
Febrile convulsions, the most common seizure disorder during childhood.
Occurring between 6 months and 6 years. Precipitated by fever from:
infection/inflammation/metabolic disorders . It is not a form of epilepsy because brain is
normal.
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Febrile seizures
In most cases it is generalized tonic - clonic convulsion. and lasts a few seconds to less than 15 minutes with a loss of consciousness.
There is no preceding aura and the childmay be postictal (confused) for a short
time after the seizure is over. A strong family history of febrile
convulsions.
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Clinical Picture Febrile convulsion is divided into three main groups based on symptoms of the
seizure: Simple febrile convulsion (convulsion
occur in majority of the cases ~ 75%, lasting less than 15 minutes , not having focal features, single in 24 hours).
Complex febrile convulsion: represent 25% of the cases, lasting more than 15 min, with focal features, multiple in 24 hours.
Febrile status epilepticus.
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Treatment of Febrile Seizures
A careful search for the cause of the fever. Use of antipyretics. Reassurance of the parents. Prolonged anticonvulsant prophylaxis for
preventing recurrent febrile convulsions is controversial and no longer recommended.
Oral diazepam, 0.3 mg/kg/8h or (1mg/kg/24hr), is administered for the duration of the illness (usually 2–3 days).
Vaccination is not contraindicated. No treatment is effective in decreasing risk of
future epilepsy.
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Counseling of the Parents
Parents should be informed about the benign nature of febrile convulsion and that it
may recure. Parents should be taught to manage the
convulsion by placing the child in recovery position (lying in his or her side to prevent aspiration and control fever).
After the seizure subsides, parents should sponge the child with tepid water to reduce the fever quickly.(applying alcohol or cold water is not advisable, because extreme cooling cause shock to an immature nervous system)
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Epilepsy
Epilepsy is a group of syndromes characterized by recurring seizures.
seizure is an involuntary contraction of muscle caused by abnormal electrical brain discharges.
Epilepsy can be primary (idiopathic)or secondary, when the cause is known and
the epilepsy is a symptom of another underlying condition such as a brain tumor
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Classification of Epileptic Seizures (recurrent
seizures) Partial (Focal) seizures:
Simple partial seizures (no altered level of consciousness)
Simple partial seizures with motor signs (include aversive, rolandic, and jacksonian march).
Simple partial seizures with sensory signs.
Complex partial (psychomotor) seizures (some impairment or alteration in level of consciousness)
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Classification of Epileptic Seizures (recurrent
seizures) Generalized seizures
Generalized tonic – clonic seizure (Grand Mal) Absence seizures (Petit Mal). Atonic seizures (Drop Attacks) Myoclonic seizures. Akinetic seizures Infantile spasms
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Partial (Focal) Seizures
Simple partial seizures with motor signs:
It arises from the area of the brain that controls muscle movement. A common motor seizure in children is:
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Partial (Focal) Seizures
i) Aversive seizure: the eye or eyes and head turn away from the
side of the focus. In some children the upper extremity toward
which the head turns is abducted and extended. The fingers are clenched giving the impression
that the child is looking at the closed fist. The child may be aware of the movement.
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Partial (Focal) Seizures
ii) Rolandic seizure: Tonic- clonic movements involving the
face. Salivation. Arrested speech. Most common during sleep. It is the common form.
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Partial (Focal) Seizures
iii) Jacksonian March: Consists of orderly, sequential
progression of clonic movements that begin in a foot, hand, or face, and as electric impulses spread from the irritable focus to contiguous regions of the cortex, move or march body parts activated by these cerebral regions.
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Partial (Focal) Seizures
2. Simple partial seizures with sensory signs:
Characterized by various sensations including numbness, tingling, prickling, or pain that originates in one area e.g. face or extremities and spreads to other parts of the body.
Visual sensations or formed images, hallucinations, tight flashes, tastes, smells, or sounds may be experienced.
Autotonic activity may include pallor, sweating, flushing, and pupil dilation.
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Partial (Focal) Seizures3. Complex Partial Seizures (Psychomotor Seizures)Vary greatly in extent and symptoms and tend
to be the most difficult type to control. Are observed more often in children from 3
years of age through adolescence. May begin with a slight aura in the form of
sensation of strange feeling at the bottom of the stomach that rises toward the throat.
This feeling may be accompanied by unpleasant odors or taste, complex auditory or visual hallucinations.
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Partial (Focal) Seizures
Cont.. Impaired consciousness ; the child may
appear dazed and confused and be unable to respond when spoken to or to follow instruction.
Automatisms (repeated activities without purpose and carried out in a dreamy state), such as oropharyngeal activities as chewing, drooling, or swallowing.
Ambulatory activities as wandering or running and verbal manifestations such as repeating word.
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Generalized Seizures I- Tonic - Clonic Seizures:
(Grand Mal) It is consisting of four stages:A- prodromal period of hours or days.B- an aura, or warning, immediately before
the seizure.C- the tonic-clonic stageD- postictal stage.* Not all four stages occur with every seizure.
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cont..
A- prodromal period of hours or days.May consist of drowsiness, dizziness, malaise,
lack of coordination, or tension. B- an aura, or warning, immediately before
the seizure.May reflect the portion of the brain in which
the seizure originates. Smelling unpleasant odors denotes activity in the medial portion of the temporal lobe. Seeing flashing lights suggests the occipital area. Repeated hallucination arise from the temporal lobe.
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cont..
C- the tonic-clonic stageTonic phase: rolling of the eyes upward immediate loss of consciousness stiffness in the entire body muscles, and the child
falls to the ground. arms usually flex, whereas the legs, head and
neck extend. lasts approximately 10 to 20 seconds the child is an apnea and may become cyanotic Autonomic stimulation causes increased salivation.
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cont..
Clonic phase: intense jerking movements as the trunk
and the extremities undergo rhythmic contraction and relaxation.
child may foam at the mouth and incontinent of urine and feces.
It lasts about 20 to 30 seconds up to 30 miutes.
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cont..D- postictal stage Falls into a soundly sleep for 1 to 4 hours
and will rouse only to painful stimuli during this time.
Child may have visual and speech difficulties and may vomit or complain of severe headache.
The child has no memory of the seizure.
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2- Absence Seizures: (Petit Mal)
Occur more frequently in girls than boys Onset of absence seizures is abrupt and the child
suddenly develops up to 100 attacks daily. Brief loss of consciousness with minimal or no
alteration, usually consist of a staring spell that lasts for a few seconds.
Rhythmic blinking and twitching of the mouth or an extremity may accompany the staring.
The sudden -rest of activity and consciousness is not accompanied by incontinence, and the child has amnesia for the episode.
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cont..
Slight loss of muscle tone may cause the child to drop objects, but he can maintain postural control.
usually lasts approximately 5 to10 seconds. usually have normal intelligence, however, if
they have frequent episodes, they may be doing poorly in school because they are missing instructional content.
Petit mal seizures can be precipitated by hyperventilation, fatigue, hypoglycemia, stresses (emotional and physiological) or sleeplessness.
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3- Atonic Seizures: (Drop Attacks)
Manifested as a sudden, momentary loss of muscle tone. Onset is usually between 2 and 5 years of
age. During a mild seizure the child may simply
experience several sudden brief head drops. During a more severe episode, the child will
suddenly fall to the ground and will lose consciousness briefly and after a few seconds will get up as if nothing happened.
Frequent falls can result in injury to face, particularly the chin, eyebrow and nose area.
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4- Myoclonic seizures: Include sudden, brief contractions of a muscle or group of muscles. No loss of consciousness or postical state. Myoclonus often appears normally in the
course of falling asleep. May be confused with the exaggerated startle
reflex, but may be distinguished by placing one's palm against the back of the child's head, if it is possible to push the child's head forward, this indicates an exaggerated startle reflex. In case of a myoclonic seizure, the child's head resists attempts to bring head forward.
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5- Akinetic seizures:
Are characterized by lack of movement, however muscle
tone is maintained so the child freezes into position and doesn't fall. If the child is lying down, the evaluation of muscle tone helps to differentiate between the atonic and Akinetic type seizure. There is impairment or loss of consciousness
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6- infantile spasm:(unclassified seizures)
characterized by Very rapid movements of the trunk with
sudden strong contractions of most of the body, including flexion and adduction of the limbs.
The infant suddenly slumps forward from a sitting position or falls from a standing position.
These episodes may occur singly or in clusters as frequently as 100 times a day.
Most common during the first 6 months of life Apparently result from a failure of normal
organized electrical activity in the brain.
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6- Infantile Spasm:(unclassified seizures)
the seizures may accompany a preexisting form of neurologic damage. In approximately 50% of those affected, there is an identifiable cause such as trauma or a metabolic disease. In the other 50%, there may be no identifiable cause.
Approximately 90% of these infants are developmentally delayed
In infants whose development was previously normal, intellectual development appears to halt and even regress after seizures start.
The infantile seizure phenomenon seems to “burn itself out” by 2 years of age but the associated cognitive or developmental delay remains.
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Diagnostic Evaluation:Has two major aims:1. To identify the type of seizures the child has
experienced, their frequency and severity, and the factors that precipitate them
2. To attempt to understand the cause of it. It includes:i. Perform complete history, physical
examination and neurologic examination, ii. Rule out metabolic causes with measurements
of serum glucose and electrolytes.
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Diagnostic Evaluation:
iii. Electroencephalography (EEG) records electrical activity of brain.
iv. Radiographic examination identifies cranial abnormalities.
v. Single photon emission computed tomography (SPECT).
It is useful for identifying the epileptogenic zone so that the area in the brain giving rise to seizures can be removed surgically
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Abnormalities in the EEG usually continue between seizures or, if not apparent, may be elicited by hyperventilation or during sleep.
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Treatment of Epilepsy principles
Drug treatment should be regular Simple as possible Minimum of side effects Monotherapy Changes should be made gradually High initial dosages increases side effects Rapid withdrawal carries the risk of provoking
status Always calculate the dosage according to the
weight
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SEIZURE PRECAUTIONS
Extent of precautions depends on type, severity, and frequency of seizures
May include: Siderails raised when child is sleeping or
resting Siderails and other hard objects padded Waterproof mattress/pad on bed/crib Appropriate precautions during potentially
hazardous.
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SEIZURE PRECAUTIONS
Swimming with a companion Use of protective helmet and padding
during bicycle riding. Supervision during use of hazardous
machinery/equipment Have child carry or Wear medical
identification Alert other caregivers to need for any
special precautions
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Status Epilepticus Refers to a seizure that lasts continuously for
longer than 30 minutes or a series of seizures from which the child doesn’t return to his or her level of consciousness.
Three major subtypes: prolonged febrile seizures idiopathic status epilepticus symptomatic status epilepticus
Severe anoxic encephalopathy in first few days of life.
The relationship between the neurologic outcome and the duration of status epilepticus is unknown in children.
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Complications
It is emergency situation that need immediate treatment
Hypoxemia Acidemia Glucose alterations Blood pressure disturbances Increased intracranial pressure High Morbidity
Neurologic sequelae Focal motor deficits Mental retardation Behavioral disorders Chronic epilepsy Acute and chronic MRI changes
High mortality (3-4%)
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Prolonged seizures
Duration of seizure
Life threatening
systemicchanges
DeathTemporary
systemicchanges
Be kind to the old for someday you'll be one of
them.