Direction of Pediatric Neurology of Pediatric Department of Tbilisi

State Medical University

Tests in Pediatric Neurology
//// The cause of seizures in early childhood is:
// Deficiency of Piridoxine
/// Deficiency of Calcium Panthothenate
/// Excessive amount of Riboflavine
/// Deficiency of Folium acid
//// The most frequent reason of epilepsy in childhood is:
/// Neurosis
// Residual encephalopathy
/// Allergy
/// Poor feeding
//// The triggering factors of epilepsy in early childhood is following, except:
/// Infection
/// Trauma
/// Radiation
// Poor nursing
//// The simple absence is defined as:
// Brief loosing of consciousness
/// Abrupt dropping
/// Tonic-clonic seizures without losing of consciousness
/// Involuntary urination and defecation
5//// West syndrome usually occurs in:
/// Neonate period
// Up to 1 year of age
/// School period
/// Pre-school period
6//// The transient Todds paresis is associated with:
/// Generalized epilepsy
/// Simple absence
/// Complex absence
// Partial epilepsy
7/// By means of electroencephalography we can not:
/// Establish the diagnosis of epilepsy
/// Define the localization of epileptic foci
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/// Assess the efficiency of therapeutic management

// Define the etiology

8//// The following drugs are recommended for the treatment of absences:
// Succinimides and Valproic acid
/// Hidantoins
/// Barbiturates
/// Carbamazepine
9//// Lennox-Gastaut Syndrome is defined as:
// Frequent, sometimes serial polymorphic seizures with mental retardation.
/// Only febrile seizures
/// Only partial seizures
/// Disease with benign course
//// The following drugs are recommended for the treatment of West syndrome:
// Hormones and Valproic acid or Vigabatrine
/// Phenobarbital
/// Diphenine
/// Diazepame
//// Generalized epilepsies are the following, except:
/// Absences
/// Myoclonic seizures
/// Tonic-clonic seizures
// Jacksons motor seizures
//// Partial seizures are the following, except:
/// Idiopathic ( age-related)
/// Symptomatic
/// Cryptogenic
// West syndrome
//// EEG pattern of typical absences is:
/// Temporal sharp waves
// 3 Hz. Spike-wave complexes
/// High amplitude generalized activity
/// 5-6 Hz. Spike-wave complexes
//// The typical EEG pattern of West syndrome is:
// Hypsarrhythmia
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/// Focal slow wave activity

/// 3 Hz. Spike-wave complexes
/// Only sharp waves

//// The typical EEG pattern of Juvenile absence epilepsy is:

/// Diffuse slow wave activity
// Generalized bilateral synchronous 3,5-4 Hz. Spike-wave complexes.
/// Low amplitude activity
/// Hypsarrhythmia
//// The typical EEG pattern of atypical absence is the following:
/// Diffuse slow wave activity
// 0,5-2,5 Hz. Spike-wave complexes
/// Hypsarrhythmia
/// Focal slow wave activity
//// The simple partial seizures are the following, except:
/// Motor
/// Clonic
// Absences
/// Vegetative
//// The preserved consciousness is the sign of:
/// Lennox-Gastaut syndrome
/// West syndrome
/// Absences
// Simple partial seizures
//// The following are not related to generalized seizures:
/// Abrupt onset
/// Progressive seizures
// Preserved consciousness
/// Amnesia of seizure episode
//// The following are related to the typical absences:
// Abrupt onset
/// The gradually onset
/// 0,5-2,5 Hz. Spike-wave complexes
/// Duration of seizures 30 seconds and more

//// The following is related to atypical absences:

/// Abrupt onset
// The gradually onset
/// 3-3,5 Hz. Spike-wave complexes
/// Duration of seizures less than 15seconds
//// Aura can be:
/// Visual
/// Auditory
/// Gustatory
// All of them
//// Febrile seizure can occur:
// Before 6 years of age
/// 6-12 years of age
/// Puberty period
/// Up to 20 years of age
//// Simple febrile seizure is not characterized by:
/// Duration < 15 minutes
// Repetition rate 24 hours
/// Rare episodes
/// Absence of neurological symptoms after seizure
//// Simple febrile seizure is characterized by:
/// Duration > 15 minutes
/// Focal paroxysm
/// Repetition rate 24 hours
// Rare episodes
//// Complex febrile seizure is characterized by:
/// Duration < 15 minutes
// Duration > 15 minutes
/// Rare episodes
/// Preserved consciousness in ictal period
//// Complex febrile seizure is not characterized by:
// Rare episodes
/// Duration > 15 minutes
/// Repetition rate 24 hours
/// Focal paroxysms

//// Absence seizure is:

/// Adversive seizure
/// Tonic seizure
/// Tonic-clonic seizure
// West syndrome
//// Absence seizure is not:
/// West syndrome
// Adversive seizure
/// Lennox-Gastaut syndrome
/// Salaami seizures
//// Partial seizures can not be:
/// Adversive
/// Tonic
/// Clonic
// West syndrome
//// Infantile spasms can occur:
/// 3 years of age
// 3-7 months of age
/// In neonatal period
//// In puberty period
//// Infantile spasms first was described by:
/// Lennox
/// Gastaut
// West
/// Jackson
//// Infantile spasm is defined as:
// Flexor-extensor spasms, mental retardation, hypsarrhythmia on EEG
/// Normal psychomotor development
/// Simple partial seizures
/// 3 Hz. Spike-wave activity on EEG.
//// Infantile spasms occur during the following conditions:
// Severe damage of CNS
/// Hyperthermia
/// Intoxication
/// Infection

//// The recommended daily dosage of ACTH for infantile spasm is:
/// 20-30 unit
// 80-100 unit
/// Less than 10 unit
/// 5 unit
//// The initial dosage of Prednisolone used for the treatment of infantile spasms is:
// 2 mg/kg/d
/// 0,5 mg/kg/d
/// 4 mg/kg/d
/// 1 mg/kg/d
//// The reduction of dosage of hormones in infantile spasms can be started:
/// When seizures become rare
// After cessation of seizures and hypsarrhythmia on EEG
/// After improving the psychomotor functioning
/// After improving the EEG patterns
//// The drug used in infantile spasms is:
// High doses of Piridoxine
/// Vitamin C
/// Vitamin D
/// Vitamin E
.//// The drug not recommended for the treatment of infantile spasms is:
/// ACTH
/// Immunoglobulin
/// Piridoxine
// Nivalin
//// The drug not recommended for the treatment of infantile spasms is:
/// Nivalin
// ACTH
/// Phenobarbital
///Piracetam
41 The complex absence is not characterized by:
// Abrupt onset
/// Tonic component
/// Clonic component
/// Gradual onset

42 The simple absence is characterized by:

/// Fixation of gaze
// Vegetative manifestation
/// Abrupt beginning and finishing
/// d. Absolutely impaired consciousness
43 The simple absence is characterized by:
/// Gradual beginning and finishing of paroxysms
/// Duration of seizure more t5han 30 seconds
/// Mioclonic component
// Abrupt cessation of motor activity
44 The complex partial seizure is characterized by:
/// Preserved consciousness
// Complete or incomplete loss of consciousness
/// Only motor component
/// Absence of amnesia
45 Generalized tonic-clonic seizure is not characterized by:
/// Loss of consciousness
/// Abrupt dropping
// Preserved consciousness
/// Tonic-clonic stage
46 Neonatal seizure occurred:
/// After 1 month of age
// 1-4 weeks of age
/// 2-4 months of age
/// After 1 years of age
47 The cause of neonatal seizures are the following, except:
/// Hypoxic-ischemic damage of CNS
// Oppenheims myotonia
/// Intracranial hemmorage
/// Microelements imbalance
48 The cause of neonatal seizures are the following, except:
/// Intrauterinal infections
/// Piridoxine deficiency
// Verding-Hoffmans spinal amyotrophy
/// Inherited metabolic disorders

49 Neonatal seizures can not be:

/// Not manifested
/// Tonic
/// Mioclonic
// Atonic
50 The reason of seizure syndrome caused by calcium deficiency are the following, except:
/// The low level of parathyroid hormone
// High level of bilirubin in blood
/// Disorder of vitamin D metabolism
/// Hypomagnemia
51 Epileptic status is defined as:
/// Normal consciousness between paroxysms
// Permanent paroxysms with duration of 30 minutes or more
/// Amnesia of seizure episode
/// Arterial hypertonia
52 Epileptic status is not defined as:
/// Permanent paroxysms with duration of 30 minutes or more
/// Amnesia of seizure episode
// Normal consciousness between paroxysms
/// Epileptic patterns on EEG
//// The management of epileptic status does not imply:
/// Monitoring of vital functions
/// Urgent anticonvulsive therapy
/// Express diagnosis
// Per os administration of anticonvulsants
//// The following drugs are recommended for the management of epileptic status:
// Diazepam or Lorazepam
/// Succinimedes
/// Lamotrigine
/// Vigabatrine
//// The drug not recommended for the management of epileptic status is:
/// Phenobarbitale 10mg/kg
/// Pentobarbitale 6-8 mg/kg
/// Lidocaine 1-2 mg/kg
// Lamotrigine 2,5 mg

//// The drug not recommended for the management of epileptic status is:
/// Diazepame or Lorazepam
/// Phenitoine
// Vigabatrine
/// Phenobarbitale
//// The drug administration in epilepsy lasts for:
/// 1-3 months
/// 3-6 months
// 3-5 years
/// 1 years
58//// The anticonvulsive therapy is conducted:
/// As a short period course for 1-2 years
// Permanently, with administration of drug for several years
/// By using of broad spectrum anticonvulsant for 6 months
/// By administration of drug for 1 year
59//// The anticonvulsive therapy is recommended to start by:
// Single anticonvulsant
/// Two or three anticonvulsants
/// Vitamins
/// Antibiotics
60 //// The drugs of first choice in febrile seizure are the following:
/// Phenobarbitale
// Valproic acid
/// Lamotrigine
/// Topiramate
61//// The drug recommended to use for the treatment of partial seizures is:
// Carbamazepine
/// Succinimide
/// B group vitamins
/// Hormone
62//// The drug not recommended to use for the treatment of partial seizures is:
/// Carbamazepine
/// Valproic acid
// Succinimnides
/// Phenobarbitale

63 The drug recommended to use for the treatment of absence seizures is:
/// Carbamazepine
/// Phenobarbitale
// Valproic acid
/// Phenitoine
64 The drug not recommended to use for the treatment of is:
/// Succinimides
/// Clonazepame
/// Valproic acid
// Carbamazepine
65 The following drugs are used for the treatment of Lennox-Gastou syndrome:
// Lamotrigine
/// Phenobarbitale
/// Piridoxyne
/// Antibiotics
66 The drugs not used for the treatment of Lennox-Gastaut syndrome is:
/// Monotherapy with Lamictal
// Phenobarbitale
/// Valproic acid
/// Clonazepame
67 The anticonvulsants of new generation is:
/// Phelbatole
/// Oxcarbamazepine
/// Acetazolamide
// Phenobarbitale
//// The basic anticonvulsant is not:
// Gabapentine
/// Phenobarbitale
/// Carbamazepine
/// Valproic acid
69 The basic anticonvulsant is :
/// Topiramate
/// Vagabatrine
// Carbamazepine
/// Midazolam

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70 Besides the drugs the approach also used for the treatment of intractable epilepsy is:
/// Physiotherapy
// Ketogenic diet
/// Occupational therapy
/// Psychotherapy
//// For the treatment of intractable epilepsy is used:
/// Electrophoresis
/// Occupational therapy
// Stimulation of Vagus
/// Psychotherapy
72 For the treatment of intractable epilepsy is used:
// Neurosurgical operations on brain
/// Occupational therapy
/// Psychotherapy
/// Electrophoresis
73 Porencephaly often causes the following form of cerebral palsy:
/// Spastic diplegia
/// Spastic tetraparesis
// Hemiparetic form
/// Hyperkinetic form
74 Aplasia of basal ganglia and nuclear jaundice cause the following form of cerebral palsy:
// Hyperkinetic form
/// Hemiparetic form
/// Spastic tetraparesis
/// Spastic diplegia
75 Littly disease is presented as the following form of cerebral palsy:
/// Spastic tetraparesis
// Spastic diplegia
/// Hyperkinetic form
/// Atonic-astatic form
76 The disorders of extremities in spastic diplegia are expressed:
/// On one side
// Disorder is symmetric
/// Upper extremities are affected more
/// Upper and lower extremities are affected on one side

//// In cerebral palsy the symmetric reflex from head to trunk and extremities is:
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/// Increased
// Is increased in neonate period and inhibited in pre-school period
/// Is absent
/// Is always changed
78 In cerebral palsy of paralitic form the muscle atrophy is expressed by the following ways:
/// Is absent
/// Occurred only in later residual period
/// Occurred only during muscle hypotonia
// Is mildly expressed and has diffuse manifestation
79 The prevalence of cerebral palsy per 1000 is:
/// 0,5 and less
// 1,5 and 2
/// 5 and more
/// 10 and more
80 In cerebral palsy of spastic tetraplegia form is expressed:
// Tetraparesis more affected the upper extremities
/// Hemiplegia on one side and hemiparesis on other side
/// Tetraparesis occurred only in severe cases
/// Disorders only in lower extremities
81 In cerebral palsy of tetraplegia form the muscle tone is:
/// Always decreased
/// Slightly increased
// Is increased significantly
/// Is increased only in later residual period
2//// In cerebral palsy of spastic diplegia form are affected:
/// Only internal capsule on one side
/// Cerebral peduncles
// Cerebral hemispheres, especially cortex
/// Brainstem
83 In cerebral palsy of spastic tetraplegic form patient start walking:
// In very rare cases
/// On the third year of life
/// After 5-6 year of age
/// Only in the case of intact mental field

4//// In cerebral palsy of hyperkinetic form is affected the following structures:

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/// The upper parts of brainstem

/// The cerebral cortex
/// Cerebellum
// Strioapidal system
//// Hearing more frequently is impaired during the following forms of cerebral palsy :
/// Spastic diplegia
/// Spastic tetraplegia
/// Hemiparetic form
// Hyperkinetic form occurring after nuclear jaundice
86//// The psychiatric disorders in cerebral palsy of atonic-astatic form occur:
/// never occur
// in case of frontal lobes disorders
/// in case of cerebellum disorders
/// in case of disorders of cerebellum pathways
7 //// The muscle tone in cerebral palsy of atonic-astatic form is changed by the following ways:
/// Spastic
/// Rigid
// Hypotonia
/// Distonia
88 The course of cerebral palsy is:
/// Progredient
// Regredient in case of adequate treatment
/// Regredient only in early period of life
/// Progredient only in preschool age
89 The prognosis of cerebral palsy depends on the following issues:
/// Only period of damage
/// Only period of starting of treatment
/// The somatic condition of child
// Time and degree of damage and period of starting of treatment
90 Contractures and deformation in cerebral palsy :
// May increase together with age
/// Is stable
/// May decrease together with age
/// May increase only in case of spastic tetraplegia
91 The epilepsy of childhood is often caused by:
/// Infection and hypotrophy
// Genetic predisposition and negative exogenous factors
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/// Minimal cerebral dysfunction

/// Defects of caring
//// The bloody saliva in epileptic seizure is the result of:
/// Nasal bleeding
/// Pharyngeal bleeding
/// Disorder of blood aggregation system
// Damage of tongue and cheeks
93 The preventive vaccination in case of epilepsy can be conducted only in the following
cases:
/// After 1-2 years from the last seizure
// After 6 months from the last seizure together with increasing the anticonvulsant
therapy
/// After 2 years from the last seizure
/// Only when the EEG patterns are normal
94 The gradual decreasing of antiepileptic treatment is possible in the following cases:
/// After 1-2 years from the last seizure
/// When there is improvement on EEG
/// Only in puberty period
// After 3-5 years from the last seizure and in case of normal EEG patterns
95 The etiological factors of neurosis is:
/// Somatic condition
/// Age
/// Premorbid background
// Psychotrauma
96 In pre- and puberty period fear is often accompanied by:
/// Hallucinations
/// Seizures
// Expressed vegetative reactions
/// Involuntary urination

//// Logoneurosis is often occurred in the following periods:

// Before 5 years of age
/// Yearly school period
/// Late school period
/// Puberty period
98 The neurogenic tics often occur in the following periods:
/// Before 3 years
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/// 3-5 years

// 5-12 years
/// After 16 years
99 The main approach in the treatment of neurosis is:
/// Physiotherapy
/// Drugs
/// Complex approach containing drugs and physiotherapy
// Psychotherapy
100 The inherited unconditioned automatism reflexes are:
/// The reflex of sucking
/// The reflex of automotive climbing
/// The reflex of grasping
// All of them
//// The following are not the reflexes of oral automatisms:
/// The reflex of sucking
/// The reflex of seeking
/// The reflex of elephant trunk
// The reflex of defense
102 The following are not the inherited myelencephalic reflexes of neonatal period:
/// The tonic symmetric neck reflex
/// The tonic asymmetric neck reflex (Magnus-Kleins)
// The reflex of grasping
/// The symmetric and asymmetric tonic reflexes
//// The sucking reflex doesnt disappear:
/// Until 2 months
/// Until 6 months
// Until 18 months
/// Until 12 months
//// The grasping (Robisons) reflex in normal neonates disappears:
/// At 2 months of age
/// At 3-4 months of age
// At 1 year of age
/// After 1 year
105 The diffuse decrease of muscle tone in neonates can occur in the following cases:
/// Damage of cerebellum
/// Werdnig-Hoffmanns spinal amyotrophy
/// Oppenheims myotonia
// Cerebral palsy of hemiparetic form
106 The feature of Werdnig-Hoffmanns amyotrophy is:

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/// Disappearance of knee reflex

/// The progredient course of disease
/// Diffuse hypotonia
// Hyppereflexia

a.

b.

107 The inherited unconditioned reflexes of neonates disappears at the following ages:
/// Before 1 month
/// Before 1-2 months
// Before 3-5 moths
/// After 1 years
//// Landau inherited reflex in neonates disappears:
/// At 1 month of age
/// At 1-3 months of age
/// At 6 months of age
// It never disappears
109 The following are not TORCH infection:
// Rubella infection
/// Cytomegalovirus infection
/// Herpes Simplex infection
/// Toxoplasmosis
//// In congenital rubella infection microcephaly occurs:
/// In 100% of cases
// In 10-20% of cases
/// In 50% and more
/// It never occurs
111 Hydrocephaly, enophthalmy, spastic paresis, epileptic seizures, chorioretinitis associated
with fetal hepatitis in neonates are the features of:
/// Rubella infection
// Toxoplasmosis
/// Cytomegalovirus infection
/// Listeriosis
//// The most frequent form of developmental defect of brain is:
/// Myelocele
/// Macrocephaly
// Microcephaly
/// Dysostosis of skull and face
113 Microcephaly is divided by the following ways:
// Primary and secondary
/// Congenital and acquired
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/// Postinfectious and posttraumatic

/// Diffuse and focal
114 In microcephaly occur the following processes:
/// The brain is significantly small in size compared to skull
// The small size skull is correlated to reduced size brain
/// Only brain part of skull is reduced compared to face part
/// The face and brain part of skull are proportional
115 Morphological determinant of microcephaly is:
/// The proportionally reduction of the whole brain
// The severe defects of development
/// Only macro- and microgyria
/// Only disorder of skull
//// The secondary microcephaly occurs in:
/// Prenatal period
/// Only postnatal period
// Perinatal period and in the first months of life
/// Any age
117 The sizes of skull in microcephaly at the moment of birth is:
/// Always reduced by 3-4 cm
/// Reduced by 5 cm and more
/// May be increased
// May be normal
//// The motor development in microcephaly is:
/// Always normal
// Is always delayed
/// Is delayed in case of combination with cerebral palsy
/// Is delayed only in primary microcephaly
9 The prognosis of microcephaly can be predicted by:
/// The rate of increasing of skull sizes
/// Skull sizes
// The level of mental retardation
/// The time of adequate treatment
The increasing of intracranial pressure is the sign of:
// Craniostenosis
/// Primary microcephaly
/// Secondary microcephaly
/// Microcephaly associated with epilepsy

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121 The spontaneous compensation of congenital hydrocephaly may occur:

/// By improving the cerebrospinal fluid absorption
// During the atrophy of choroidal plexuses and by reducing the cerebrospinal fluid
production
/// By moving away of skull sutures
/// During the liquorrhea
122 Hydrocephaly:
/// Is always secondary and is the result of brain atrophy
/// Is always primary
// May be primary or secondary
/// Always occurs during porencephaly
//// In congenital hydrocephaly the following changes occur on the fundus of eye:
/// Congestion
/// Angiopathy
// The decoloration of optic disk
/// The neuritis of optic nerve
124 The non-compensating hydrocephaly occurs:
/// Only during the viral infection
/// Only during the enterovirus infection
/// Only during the neuroinfection
// During the CNS trauma or infection
//// The surgical treatment of hydorcephaly is recommended in order to:
/// Improve venous circulation
/// Normalize the cerebral hemodinamics
// Make the collateral circulation of cerebrospinal fluid
/// Reduce the secretion of cerebrospinal fluid
//// The perinatal period is defined as the period:
/// From the first movement of fetus to moment of birth
// From 28 weeks of gestation to first 7 days of life
/// From 28 weeks of gestation to moment of birth
/// The first 7 days of life
127 The traumatic injury of spinal cord in neonates often occurs in the following segments:
/// The upper cervical
// Intumenscentia cervicalis
/// Thoracal
/// Intumenscentia lumbaris
//// The obstetrical paralysis of hand of total type occurs during the damage of the following
segments:
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/// C5-C6
/// C7-C8
/// D1-D2
// C5-D1
//// The obstetrical paralysis of hand of proximal type occurs during the damage of the following
segments:
// C5-C6
/// C7-C8
/// D1-D2
/// C5-D1
130 The obstetrical paralysis of hand of distal type ( Dejerin-Klumpke) occurs during the
damage of the following segments:
/// C5-C6
/// C7-C8
// D1-D2
/// C5-D1
131 The structural defect of the brain in cerebral palsy affects the following functions:
/// Only motor development
/// Only speech development
// The development of the whole brain
/// It doesn't affect on brain development
//// The cerebral palsy in relation to hypoxic-ischemic encephalopathy is:
/// Independent disease
/// Ordinary outcome
/// The have no relation
// One possible variant of outcome
133 In cerebral palsy of spastic diplegia form occurs:
/// Upper spastic paraparesis
/// Spastic hemiparesis
// Lower paraparesis
/// Tetraparesis
//// The spastic tetraparesis form of cerebral palsy is defined as:
/// Tetraparesis with mild mental retardation
// Tetraparesis with severe mental retardation
/// The peripheral paresis in hands and spastic paresis in legs
/// The spastic paresis in hands and peripheral paresis in legs
135 In cerebral palsy of atonic-astatic form are impaired the following structures:
/// Both internal capsules
/// Basal ganglias
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// Cerebellum
/// The brain hemispheres
//// The possible reason of traumatic injury of facial nerve in neonates is not:
/// Face presentation
/// Difficult labor
/// The fractures of temporal bone
// Subarachnoidal hemmorage
//// The reason of spinal cord trauma can be:
// Pelvic presentation
/// Cross birth
/// Normal cephalic presentation
/// Brow presentation
//// The spinal injury in neonates occurs in the following cases:
/// Intrauterine hypoxia
/// Natal period asphyxia
/// Natal period infection
// Natal period trauma
//// The severe damage of CNS can be defined by Apgar's scale by the following scores:
/// 0-1
// 1-4
/// 5-6
/// 6-7
140 The moderate damage of CNS can be defined by Apgar's scale by the following scores:
/// 0-1
/// 1-4
// 5-6
/// 6-7
//// The mild damage of CNS can be defined by Apgar's scale by the following scores:
/// 0-1
/// 1-4
/// 5-6
// 6-7
142 The etiological factor of hypoxic-ischemic encephalopathy is not:
/// Hypoxia
/// Trauma
/// Toxic process
// Congenital factor

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//// The good prognosis has the following form of hydrocephaly:

/// Occlusive
// Open, with slow rate of progression
/// Occurring during intrauterine infections
/// Occurring after delivery trauma
144 The mental retardation in severe hydrocephaly is presented by the following ways:
/// Severe retardation
// Ranging from mild form to idiotia
/// Often in normal range
/// Slightly expressed retardation
//// The reason of Grephe's symptom in hydrocephaly is the following:
/// The irritation of cilliospinal sympathic nucleus
/// Defects of vision
/// Increasing of intraorbital pressure
// Deformation of orbitas and exophthalmus

146 The head circumference starts to increase in the following periods:

// The first month of life
/// 3-5 months of life
/// After 6 months of life
/// At 1 year of life
//// The following conditions occur in severe hydrocephaly:
/// Optical nerve neuritis
// Hydroanencephaly
/// Pyramidal deficiency
/// Lesion of cerebellum and its connections
//// The most frequent reason of congenital hydrocephaly is:
/// Porencephaly
/// Agenesia of corpus callosum
/// Aplasia of cerebellum
// Occlusion of cerebral aquaductus
149 The child with congenital hydrocephaly may has:
// Normal or slightly increased head circumference
/// Increased head circumference by 4-5 cm
/// Reduced circumference of head
/// Increased head circumference by 5-8 cm
//// The most frequent form of hydrocephaly is:
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/// Traumatic
/// Toxic
/// Hypoxic
// Congenital
151 Dilatation of subarachnoid spaces occurs in the following forms of hydrocephaly:
/// Internal
// External
/// Basal
/// Convexital

//// Dilatation of brain ventricles and subarachnoid spaces occurs in the following forms of
hydrocephaly:
/// Internal
/// External
// Open
/// Convexital
153 Dilatation of only ventricles occurs in the following forms of hydrocephaly:
// Internal
/// External
/// Basal
/// Convexital
//// By the period of development hydrocephaly can be divided in the following forms:
/// Primary and secondary
// Congenital and acquired
/// Pre- and postnatal
/// Early ( before 6 month) and late ( after 6 month)
//// Passive hydrocephaly occurs in the following cases:
// Brain atrophy or progressive sclerosis of brain
/// Disorder of cerebrospinal fluid absorption
/// Venous stasis
/// Excessive production of cerebrospinal fluid
156 The basic sign of hydrocephaly is:
/// Increasing of intracranial pressure
// Imbalance between the production and absorption of cerebrospinal fluid
/// Dilatation of ventrical system and cerebrospinal circulation ways
/// Increased head circumference
//// The clinical feature of hypertensive-occlusive crisis implies:
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// Common cerebral hypertensive signs and focal neurological symptoms

/// Meningeal signs
///Generalized seizures
/// Only focal signs
//// The reason of hypertensive-occlusive crisis is:
/// Excessive production of cerebrospinal fluid
// Occlusion of cerebrospinal fluid circulation ways
/// Subarachnoid hemmorrage
/// Difficulty of cerebrospinal fluid absorption
//// The X-ray signs of hydrocephaly are not:
/// Atrophy of skull bones
/// Flattening of skull base bones
/// Dilatation of sella turcica
// Existence of intracranial calcification
Head of Neurological Direction
of Pediatric Department of
Tbilisi State Medical University,
Professor

Nana Geladze

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