This document provides an overview of organic brain disorders including the definition, clinical features, etiology, diagnosis, and management. Some key points: - Organic brain disorders are caused by primary brain pathology or secondary brain dysfunction due to systemic disease. Common causes include neurodegenerative disorders, vascular disorders, infections, tumors, and toxic/metabolic disorders. - Delirium is characterized by acute onset of confusion and impaired consciousness. Dementia is a chronic disorder characterized by cognitive decline over months to years. Organic amnestic syndrome specifically involves memory impairment. - Evaluation involves medical history, physical/neuro exam, and lab/imaging tests to identify underlying causes. Treatment focuses on correcting any reversible causes as

1. Organic Brain Disorders
Vinnci Angelica G. Dela Cruz
BS Psychology III
September 30, 2014

2. Why organic?

3. 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

4. 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

5. Definition
• Acute Organic Brain Syndrome
– Delirium
• Chronic Organic Brain Syndrome
– Dementia

6. 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

7. Etiology
•Alzheimer’s disease
• Parkinson disease
•Lewy body dementia
Degenerative
•Pseudodementia of depression
• Cognitive decline in late life scizophrenia Psychiatric
Vascular •Multi infarct dementia
Demyelinating • multiple sclerosis
• Vitamin def (e.g vit B12,folate),
endocrinopathies (eg hypothyroidism),
abnormality of cortisol metabolism
Metabolic

8. Etiology
• Prion disease ( Creutzfeld –Jakob disease)
• AIDS Infection
• Alcohol, heavy metals, irradition,
pseudodementia d2 medication
(anticholinergics), carbon monoxide
Drugs and
toxins
• Huntington disease, trauma(dementia
pugilistica in boxers), tumor Others

9. 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

10. 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
ILLUSIONS
HALLUCINATIONS
Mostly Visual
INSOMNIA
DAY TIME SLEEPINESS

11. 7. Sun Downing – six in evening
8. 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 MEMORY
SLURRING of SPEECH
INCOHERANCE

12. 12
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

13. Organic ETIOLOGY of Delirium
CLASS 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/SUBSTANC
E
(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

14. 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

15. • 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

16. DELIRIUM VS DEMENTIA

17. B. DEMENTIA

18. • 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

19. 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

20. • 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

21. Types and causes Of Dementia
TYPE CAUSES
Parenchymato
us 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
Commonest: ALZHEIMERS DEMENTIA, MULTIINFARCT DEMENTIA, HYPOTHYROID
DEMENTIA, AIDS DEMENTIA COMPLEX
IOP ↑ Brain tumor, Headinjury hematoma, hydrocephalus

22. 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

23. MANAGEMENT OF DEMENTIA
Non-pharmacologica
l
Pharmacological Caregivers
Cognition Behaviour Mood Intervention
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
Multicomponen
t intervention:
•Psychotherapy
•Psychoeducatio
n
•Supportive
therapy
•Respite/day
care
•training

24. 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

25. 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

26. • 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)

27. 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

28. 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

30. 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)

31. • 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

32. 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

33. 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

34. 2014/9/28

35. 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)

36. • The Lesions include:
• Head trauma
• Surgical procedure
• Hypoxia
• Posterior cerebral artery stroke
• Herpes simplex encephalitis

37. 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

38. D. Other Organic Mental
Disorders
• Organic Hallucinosis
• Organic Catatonic Disorder
• Organic Delusional (Schizo like) disorder
• Organic Personality Disorder

39. Organic Hallucinosis
• Etiology:
• Drugs:Hallucinogens,cocaine,cannabis,bro
mide)
• Alcohol:In alcoholic hallucinosis,auditory
hallucinations are more common
• Migraine
• Epilepsy: Complex partial seizures
• Brain stem lesions

40. • 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.

41. 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

42. Management
• Treatment of underlying cause
• Symptomatic treatment with low doses of
benzodiazipam or an anti-psychotic or
electro convulsive therapy.

43. 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

44. Management
• Treatment of underlying cause
• Symptomatic treatment with low doses of
benzodiazipam or an anti-psychotic or
electro convulsive therapy.

45. CONVULSIVE DISORDES
45

46. 46
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

47. Etiology of Seizures in
47
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.

48. Etiology of Seizures in
48
Children
 B) Chronic/Recurrent :
(i) with fever: recurrent febrile
convulsion.
(ii) without fever: epilepsy.

49. 49
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.

50. 50
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 child
may be postictal (confused) for a short time
after the seizure is over.
 A strong family history of febrile convulsions.

51. 51
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.

52. 52
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.

53. Counseling of the Parents
 Parents should be informed about the
benign nature of febrile convulsion and that it may
53
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)

54. 54
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

55. Classification of Epileptic
Seizures (recurrent seizures)
55
 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)

56. Classification of Epileptic
Seizures (recurrent seizures)
56
 Generalized seizures
 Generalized tonic – clonic seizure
(Grand Mal)
 Absence seizures (Petit Mal).
 Atonic seizures (Drop Attacks)
 Myoclonic seizures.
 Akinetic seizures
 Infantile spasms

57. 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:
57

58. Partial (Focal) Seizures
58
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.

59. 59
Partial (Focal) Seizures
ii) Rolandic seizure:
 Tonic- clonic movements involving the face.
 Salivation.
 Arrested speech.
 Most common during sleep.
 It is the common form.

60. 60
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.

61. 61
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.

62. 62
Partial (Focal) Seizures
3. 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.

63. Partial (Focal) Seizures
63
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.

64. 64
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 stage
D- postictal stage.
* Not all four stages occur with every seizure.

65. 65
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.

66. 66
cont..
C- the tonic-clonic stage
Tonic 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.

67. 67
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.

68. 68
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.

69. 69
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.

70. 70
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.

71. 71
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.

72. 72
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.

73. 73
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

74. 74
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.

75. 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.
75
 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.

76. 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
76
and neurologic examination,
ii. Rule out metabolic causes with measurements
of serum glucose and electrolytes.

77. Diagnostic Evaluation:
iii. Electroencephalography (EEG) records
electrical activity of brain.
iv. Radiographic examination identifies cranial
abnormalities.
v. Single photon emission computed tomography
77
(SPECT).
It is useful for identifying the epileptogenic zone
so that the area in the brain giving rise to
seizures can be removed surgically

78. Abnormalities in the EEG usually continue between seizures or, if not
apparent, may be elicited by hyperventilation or during sleep.
78

79. 79
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

80. SEIZURE PRECAUTIONS
Extent of precautions depends on type, severity,
80
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.

81. SEIZURE PRECAUTIONS
81
 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%)

84. 84
Prolonged seizures
Life
threatening
systemic
changes
Duration of seizure
Death
Temporary
systemic
changes

85. Be kind to the old for someday
you'll be one of them.