Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pediatrics > Neurology > Flashcards

Neurology Flashcards

1
Q

pathway of CSF circulation

A
  1. Secretion
    Choroid plexus in the ventricles (lateral ventricle mainly)
  2. Circulation —
    Lateral ventricle
    V
    Foramina of Monro
    V
    3rd ventricle
    V
    Aqueduct of Sylvius
    V
    4th ventricle
    V
    Foramen of Luschka and Magendie vessels
    V
    Subarachnoid space
  3. Absorption
    CSF is reabsorbed into venous circulation from subarachnoid spaces by arachnoid villi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

the most common congenital cause of hydrocephalus

A

Aqueduct stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Etiology of obstructive Hydrocephalus

A

Obstructive (non- communicating) hydrocephalus
1. Congenital
a. Aqueduct stenosis (the most common congenital cause): congenital stenosis or d
b. Dandy Walker malformation
Incomplete formation of the cerebellar vermis with obstruction of
foramina of Magendia and Luschka: Cystic expansion of th
ventricle with bulging occiput.
c. Vein of Galen malformation.
2. Acquired (the most common site of obstruction is at the aqueduct of Sylvius)
a. Traumatic: Posterior fossa subdural hematoma
b. Inflammatory post meningitic gliosis
c. Neoplastic: posterior fossa tumors e.g. cerebellar medulloblastoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Etiology of communicating hydrocephalus

A

Congenital: Arnold- Chiari malformation
There is Failure of pontine flexure development > downward displacement of
medulla and cerebellum obstruction of subarachnoid space around the
brain stem usually.
Meningomyelocele is present in 80% of cases.
2. Acquired
a. Traumatic: subarachnoid hemorrhage.
b. Inflammatory post meningitic subdural adhesions
c. Neoplastic: choroid plexus papilloma overproduction of CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clinical picture of Hydrocephalus

A

General examination:
3 skulls:
large head
sutures widely separated
anterior fontanelle widely opened
3 Skin
stretched skin
scalp veins: prominent
loss of hair
3 eye
sunset appearance
squint
vision impaire
back: meningocele or meningomyelocele in Chiari malformation
Neurological examination:
Spasticity, Hypertonia, Hyperreflexia, Paralysis
Delayed motor and mental development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

investigations of Hydrocephalus

A
  1. CT scan (the most important): dilatation of the ventricular system
    Obstructive hydrocephalus: dilatation only proximal to the site of obstruction
    Communicating hydrocephalus: all ventricles are dilated
  2. antenatal ultrasound screening.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment of Hydrocephalus

A

Treatment
1. Surgical
a. Removal of cysts or tumors that cause obstruction e.g. (choroid plexus papillectomy)
b. Non removable causes shunt operation: ventriculoperitoneal shunt is the most common

  1. Acetazolamide: in non-progressive cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Definition of Meningitis

A

Inflammation of the pia and arachnoid matter which might intervene with CSF circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Inflammation of the pia and arachnoid matter which might intervene with CSF circulation

A

Meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Etiology of Meningitis

A
  1. Bacterial
    a. During the first 2 months of life
    B B hemolytic streptococci
    Gram negative enteric bacilli : E coli
    Listeria monocytogenes
    b. From 2 month to 12 years
    Hemophilus influenza type B
    Pneumococci
    Meningococci
  2. Viral
    a. Enteroviruses (e.g. echo virus, Coxsackie) are the commonest.
    b. Epstein-Barr virus, adenoviruses and mumps.
  3. Tuberculous meningitis
  4. Other rare causes:
    a. Mycoplasma
    b. Fungal infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Source of infection of Acute bacterial meningitis

A
  1. Hematogenous dissemination from a distant site (nasopharynx) > choroid plexus

of the lateral ventricles > meninges and CSF.
2. Bacterial invasion from a contiguous focus (sinusitis, otitis media, mastoiditis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pathophysiology of Acute bacterial Meningitis

A
  1. Early: leukocyte infiltration and activation leading to release of inflammatory mediators. So, edema and endothelial damage and small infarctions occur.
  2. Later: fibrosis can lead to obstructive hydrocephalus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Manifestations of increased intra-cranial tension

A

In infants
1. Bulging fontanelle and separated sutures: late signs.
In older children
1. Projectile vomiting.
2. Severe headache.
3. Blurring of vision (papilledema): late sign.
4. Abducent or Oculomotor nerve paralysis.
5. Hypertension with bradycardia and irregular shallow breathing (late signs)

B23

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

clinical picture of Acute bacterial meningitis

A

F CCII F
Fever: vomiting, letharg
coma
convulsions
Increased cranial tension
Meningial irritation: DIC
Focal neurological damage

B23

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Manifestations of meningeal irritation

A
  1. Neck pain and rigidity: passive flexion of the neck is difficult and painful.
  2. Kernig’s sign: if the hip and knee joint are flexed at 90, extension of the knee will be limited.
  3. Brudzinski sign: if the neck is flexed— the hips and knees will be flexed too.
  4. Arched back (opisthotonus) : late sign

B24

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Manifestations of neurological deficits

A

spasticity
parpalysis
deafness
blindness
squint
mental retardation
convulsions
reduced consciousness or even coma.

17
Q

INV of acute bacterial meningitis

A

CSF examination
1. Differentiating bacterial meningitis from tuberculous and viral meningitis from table
2. Culture and sensitivity tests are essential: if bacterial infection is suspected
3. Detection of antigens (PCR) and antibodies (ELIZA) of viral infection
4. Ziehl-Nielsen staining of the CSF if TB meningitis is suspected
other investigations
1. CBC: marked leukocytosis with bandemia
2. Blood culture
3. Kidney functions test and electrolytes
4. Coagulation screen if DIC is suspected
5. If TB is suspected: chest X ray, tuberculin rest.
6. CT with contrast to detect meningeal enhancement
7. MRI brain for better visualization of cerebral infarcts.

17
Q

Contraindications of lumbar puncture

A
  1. Cardiopulmonary instability
  2. Coagulopathy or thrombocytopenia
  3. Coma with (GCS less than 9)
  4. Marked increased intracranial tension
  5. Infections at the site of lumbar puncture.
18
Q

Complications of Acute bacterial meningitis are common in

A

Common in pneumococcal infection than meningococcal infection

18
Q

Complications of Acute bacterial meningitis

A

A. Early complications

1.C.N.S
Subdural effusion: (confirmed by CT)
Convulsions focal or generalized.
Cerebral abscess: confirmed by CT scan.
2. others
a. Disseminated intravascular coagulopathy.
b. Shock due to acute adrenal insufficiency.
c. Inappropriate antidiuretic hormone release resulting in hyponatremia.
d. septicemia
1. Hydrocephalus due to inflammatory obstruction of CSF pathways.
2. Subdural empyema that increases the intracranial tension.
3. Epilepsy due to focal infarctions and adhesions
4. Focal Neuro deficit Signs………..

19
Q

Prevention of Acute Bacterial meningitis

A
  1. Vaccination
    a. Infants in the first year of life: HIB vaccine (against Hemophilus influenza) and pneumococcal conjugate vaccines
    b. Children: at 2-3 years of age.-Meningococcal polysaccharide vaccine
  2. Chemoprophylaxis
    Rifampicin in meningococcal nasopharyngeal carriers and household contact
20
Q

Treatment of Acute Bacterial meningitis

A

Treatment:
A. supportive: ABC
CCI
=Care of coma
=Anticonvulsants: diazepam and phenobarbitone.
= IV fluid if meningitis is complicated by shock (otherwise fluid is restricted to minimize cerebral edema
Assisted ventilation if respiratory failure occurs.
B. Specific treatment
a. Antibiotics: IV for at least 10- 14 days (in neonates 3 weeks).

Neonates and infants below 2 months:-
Third generation cephalosporins e.g. Cefotaxime 200 mg kg/day plus ampicillin 100mg/kg/day.

Infants and children above 2_months:-
Third generation cephalosporin e.g. Cefotaxime 200mg/kg/day or ceftriaxone plus vancomycin

Dexamethasone in H influenza infection to decrease incidence of gliosis and hearing loss

C. Follow up to detect late complications e.g. Epilepsy and mental retardation

B26

21
Q

Diffuse viral infection of brain parenchyma

A

Encephalitis

22
Q

the most common that causes Encephalitis

A

Herpes simplex type 1 and type 2

22
Q

Etiology of Encephalitis

A
  1. Herpes simplex type | and type Il: It causes encephalitis year-round. (sporadic) (the most common)
  2. Enteroviruses ( Echo and Coxsackie): Cause encephalitis outbreaks during summer : C8)
  3. Epstein Barr virus.
  4. Arboviruses: outbreaks during the summer (mosquitoes born) Examples: California
    encephalitis virus.
  5. Viruses associated with childhood illness; Measles, rubella, Chicken pox, and Mumps
  6. Other rare causes of encephalitis: Rabies, CMV, and HIV viruses
22
Q

Clinical picture of Encephalitis

A

F CC I F
1. Manifestations of Viremia (early features): fever, nausea, and upper respiratory symptom
2. Manifestations of increased intracranial tension less severe than meningitis: ,
3. Manifestations due to neurological deficits
« Disturbed level of Consciousness, irritability, abnormal movements, confusion up to deep coma :
» Convulsions
« Paralysis or paresis and spasticity are common..
4. Manifestations of complications (post encephalitic sequelae) may develop later on:-
« Epilepsy_due to focal adhesions with underlying cortical irritation
: Mental retardation, cerebral palsy and learning deficits
« Auditory, visual, speech and behavior abnormalities.

23
Q

Investigations for Encephalitis

A

CSF examination, CSF PCR, Culture and sensitivity and BACTEC
Serological tests: to detect antiviral antibodies PCR ELISA
Imaging
1. CT scan: reveal focal or generalized abnormalities
MRI: show foci of demyelination. In herpes encephalitis there is temporal lobe affection
2. EEG: A diffuse, bilateral slowing of background activity
In herpetic encephalitis, there might be focal lesions in temporal areas,

24
Q

Treatment of encephalitis

A

Treatment
1. Supportive: ICU management
a. Basic life support: A+B+C
b. Control of convulsions (diazepam and phenobarbitone)
c. Dehydrating measures to lower the increased intracranial tension.
a. Head elevation 30 ° in neutral position.
b. Osmolar therapy with mannitol or hypertonic saline,
c. Mechanical hyperventilation in severe cases.
2. Antiviral therapy: possible only with Herpes simplex encephalitis: Acyclovir

25
Q

brain abscess most common within

A

4-8 years

26
Q

causative organism of brain abscess

A

Staph aureus, streptococci

26
Q

multiple brain abscesses are common with

A

Meningitis

27
Q

sites of brain abcess

A

frontal, parietal and temporal lobes

28
Q

clinical picture of brain abscess

A

F CC I F
fever
coma covulsions
increased intracranial manifestations…..
focal neurological deficits……….

29
Q

Investigations of brain abscess

A
  1. Plain CT&raquo_space; rounded hypodense lesion.
  2. Contrast CT&raquo_space; the abscess capsule shows ring enhancement
30
Q

Treatment of brain abscess

A

combination of antibiotics 4-6 weeks and aspiration surgical drainage

31
Q
A

Pediatrics (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions